BAB 19

Chest Wall, Lung, Mediastinum,

and Pleura
TRACHEA
Anatomy
The trachea is composed of cartilaginous and membranous portions,
beginning with the cricoid cartilage, the first complete
cartilaginous ring of the airway. The cricoid cartilage consists
of an anterior arch and a posterior broad-based plate. Articulating
with the posterior cricoid plate are the arytenoid cartilages.
The vocal cords originate from the arytenoid cartilages and then
attach to the thyroid cartilage. The subglottic space, the narrowest
part of the trachea with an internal diameter of approximately
2 cm, begins at the inferior surface of the vocal cords
and extends to the first tracheal ring. The remainder of the distal
trachea is 10.0 to 13.0 cm long, consists of 18 to 22 rings, and
has an internal diameter of 2.3 cm (Fig. 19-1).1 Bronchoscopically,
the tracheal rings are visible as C-shaped hyaline cartilaginous
structures that provide rigidity to the anterior and lateral
tracheal walls. The open ends of the C-rings are connected by
the trachealis smooth muscle and encased in a dense band of
connective tissue called perichondrium. The first tracheal ring
is attached directly to the cricoid cartilage; there are approximately
two rings for every 1 cm of tracheal length.

The tracheal blood supply, which includes the inferior

thyroid, subclavian, supreme intercostal, internal thoracic, innominate, and superior and middle bronchial
arteries, enters
the airway near the junction of the membranous and cartilaginous
portions (Fig. 19-2). Each arterial branch supplies a
segment of 1.0 to 2.0 cm, thereby limiting circumferential mobilization
to that same distance. The vessels are interconnected
along the lateral surface of the trachea by an important longitudinal
vascular anastomosis that feeds transverse segmental vessels
to the soft tissues between the cartilages.

Tracheal Injury
Tracheal injury can result from a variety of causes, including
inhalation of smoke or toxic fumes, aspiration of liquids
or solid objects, endotracheal intubation, blunt and penetrating
trauma, and iatrogenic injury during operative procedures. Early
diagnosis is critical to avoid subsequent complications, including
respiratory infection and tracheal stenosis. Management of
smoke or toxic fume inhalation and liquid aspiration is commonly
supportive; use of antibiotics, respiratory support, and
airway clearance with flexible bronchoscopy is dictated by the
patient’s condition. In rare circumstances, extracorporeal membrane
oxygenation is required if there is associated injury to the
more distal airways and lung parenchyma.

Despite ubiquitous use of high-volume–low-pressure

cuffs, overinflation of the endotracheal cuff is the most common cause of injury secondary to endotracheal
intubation. High cuff
pressures can cause ischemia of the contiguous airway wall in
as short as 4 hours. Prolonged overinflation can lead to scarring
and stenosis; full-thickness injury can result in fistulae between
the innominate artery anteriorly and the esophagus posteriorly.
Avoidance requires careful cuff management to keep pressuresas low as possible; in circumstances of
prolonged ventilatory
support and high airway pressure, cuff pressure monitoring (to
maintain pressures <20 mmHg) is advisable.

Historically, clinically significant tracheal stenosis after

tracheostomy occurred in 3% to 12% of cases, with severe stenosis
in 1% to 2%.2 With the use of low-pressure cuffs, the estimated
incidence has decreased to 4.9 cases per million patients
per year.3 Intubation-related risk factors include: prolonged intubation;
high tracheostomy through the first tracheal ring or cricothyroid
membrane; transverse rather than vertical incision on
the trachea; oversized tracheostomy tube; prior tracheostomy or
intubation; and traumatic intubation. Stenosis is also more common
in older patients, in females, after radiation, or after excessive
corticosteroid therapy, and in the setting of concomitant
diseases such as autoimmune disorders, severe reflux disease,
or obstructive sleep apnea and the setting of severe respiratory
failure. However, even a properly placed tracheostomy can lead
to tracheal stenosis because of scarring and local injury. Mild
ulceration and stenosis are frequently seen after tracheostomy
removal. Use of the smallest tracheostomy tube possible, rapid
downsizing, and a vertical tracheal incision minimize the risk
for posttracheostomy stenosis.

Stridor and dyspnea on exertion are the primary symptoms

of tracheal stenosis. In the setting of postintubation injury, a
significant portion of the cartilaginous structural support to the
airway is destroyed by regional ischemic necrosis; during healing,
a web-like fibrous growth develops and narrows the airway
(Fig. 19-3). In contrast, stenosis caused by tracheostomy is
most commonly due to an excess of granulation tissue formation
around the tracheal stoma site. Time to onset of symptoms after
extubation or tracheostomy decannulation usually ranges from
2 to 12 weeks, but symptoms can appear immediately or as long as 1 to 2 years later. Frequently, patients
are misdiagnosed as
having asthma or bronchitis, and treatment for such illnesses can
persist for some time before the correct diagnosis is discovered.
Generally, symptom intensity is related to the degree of stenosis
and to the patient’s underlying pulmonary disease.