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Costal Cartilage Tracheoplasty for Congenital Long-Segment Tracheal Stenosis
James W. Forsen, Jr, MD;
Rodney P. Lusk, MD;
Charles B. Huddleston, MD
Arch Otolaryngol Head Neck Surg. 2002;128:1165-1171.
ABSTRACT
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Objectives To evaluate and report the outcome of costal cartilage tracheoplasty
for the treatment of congenital long-segment tracheal stenosis.
Design Retrospective chart review.
Setting Academic tertiary care children's hospital.
Patients Consecutive series of 10 patients who presented with congenital long-segment
tracheal stenosis.
Intervention All patients underwent costal cartilage tracheoplasty while receiving
cardiopulmonary bypass.
Measurements Age at repair, weight at repair, length of stenosis, minimal diameter
of stenosis, postoperative days receiving ventilator support, postoperative
days until discharge, postoperative bronchoscopies, postoperative complications,
associated anomalies, survival rate, and current status.
Results There were 8 males and 2 females with an average age at repair of 18
weeks. Average weight was 5.2 kg. Average length of stenosis was 3.2 cm, and
average minimal diameter was 1.9 mm. Average postoperative days receiving
ventilator support was 17 with a median of 9.5. Average postoperative days
until discharge was 35.2 with a median of 17. Average postoperative bronchoscopies
was 18 with a median of 4.5. There was a 40% major postoperative complication
rate. Seven of the patients had associated anomalies. No patient died from
an inadequate tracheal airway, though 2 patients ultimately died from other
cardiopulmonary complications for a survival rate of 80%. Average time since
surgery for survivors is 8.0 years. Two patients still require treatment.
Seven of the original 10 patients are fully active without tracheostomy.
Conclusion We report one of the largest series of costal cartilage tracheoplasty
for congenital long-segment tracheal stenosis and one that has met with a
relatively high success rate.
INTRODUCTION
CONGENITAL long-segment tracheal stenosis (CLSTS) is a rare and life-threatening
disorder. By convention, the stenosis involves greater than one half of the
length of the trachea and usually involves complete cartilaginous tracheal
rings. The pathogenesis of CLSTS is poorly understood.
Congenital tracheal stenosis was first described by Gregor in 1899.1 Cantrell and Guild2 categorized
congenital tracheal stenosis due to complete tracheal rings into 3 types.
Type 1 is hypoplasia of the entire trachea with subsequent stenosis from the
cricoid to the carina. Type 2 is funnel-shaped stenosis with the narrowest
portion of the trachea located distally, near the carina. Type 3 is segmental
tracheal stenosis where the stenotic segment gives the trachea an hourglass
appearance. Any of the 3 types may result in long-segment stenosis. Type 1
is usually the most severe. There is a high association between CLSTS and
various other congenital anomalies.3 In particular,
cardiac malformations along with vascular rings and slings are common.
It is generally believed that the pediatric patient can tolerate up
to 50% narrowing of the trachea before becoming symptomatic. Stenosis greater
than 50% usually requires intervention. However, prior to the 1980s, management
of CLSTS routinely met with dismal results to the extent that some authors
recommended conservative treatment.4 In the
last 20 years, numerous changes have occurred that have cumulatively resulted
in a dramatic improvement in the prognosis for patients with these complications.
Education has led to heightened clinical awareness so that the entity of CLSTS
is better understood and recognized earlier. Technological improvements, particularly
with the development of fiberoptic telescope and bronchoscope systems, have
allowed for more accurate diagnoses and safer airway management. Better anesthetic
techniques and improved cooperation between anesthesiologist and surgeon have
evolved. All of the advances have subsequently allowed for the development
of more aggressive and successful surgical interventions.
The work of Grillo5 demonstrated that
stenoses involving less than half of the trachea could be managed by segmental
resection and end-to-end anastomosis. Treatment for longer stenoses has inspired
a search for various materials to augment the deficient caliber of the tracheal
lumen. The ideal graft would be safe, readily available, easy to shape, biocompatible,
rigid, quickly epithelialized, and ultimately able to grow with the patient.
No single material has perfectly addressed all of these requirements. To date,
a number of augmentation tracheoplasties have been performed using synthetic
mesh,3 periosteum,3 dura,6 omentum,7 anterior
esophageal wall,8-9 pericardium,10-14 and
costal cartilage.15-20
For the past 15 years, we have treated CLSTS with costal cartilage tracheoplasty
(CCT) at our institution. Twice, we have reported our results in the thoracic
surgery literature.21-22 This
article adds several patients to our series, provides further follow-up information,
and is now presented in the otolaryngology literature.
PARTICIPANTS AND METHODS
DIAGNOSIS
The majority of the patients had been referred to the Division of Pediatric
Otolaryngology, St Louis Children's Hospital, St Louis, Mo, for evaluation
of noisy breathing or respiratory distress. Others were initially evaluated
by the Division of Pediatric Cardiothoracic Surgery for management of cardiovascular
anomalies with secondary consultation by otolaryngology.
A pediatric otolaryngologist made the diagnosis of CLSTS with a rigid
bronchoscope and with the patient under general anesthesia. The diagnosis
of CLSTS was confirmed when the stenosis involved greater than one half of
the length of the trachea. In addition to measuring the length of the stenosis,
an attempt was made to determine the narrowest diameter of the stenosis. The
minimal diameter value was obtained by sizing the stenosis with a bronchoscope
or telescope of known outer diameter. The smallest telescope had a diameter
of 1.9 mm and, in several patients, could not be passed through the narrowest
aspect of the stenosis. In these cases, the endoscopist made an estimate of
the minimal diameter of the stenosis.
SURGERY
Our technique for CCT has been described elsewhere22 and
will be reviewed here.
An otolaryngologist working in conjunction with a cardiothoracic surgeon
performed all repairs. All patients were administered general anesthesia per
endotracheal intubation. Because of compromised respiratory status, some patients
arrived in the operating room already receiving mechanical ventilation. The
otolaryngology team began by making a transverse incision through the skin
overlying the anterior aspect of one of ribs 6 through 8. The entire cartilaginous
portion of one rib was harvested with care taken to preserve the perichondrium
on the superficial surface of the rib. The deep layer of perichondrium was
left in situ to protect against entering the thoracic cavity. The harvested
graft was then fashioned to a keel shape on the back table (Figure 1). The harvest site was initially left unclosed.
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Figure 1. The costal cartilage graft is
harvested from an incision separate from the midline sternotomy. The superficial
perichondrium is left on the graft. Illustration reprinted courtesy of Mosby
Inc.22
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The cardiothoracic surgeon then performed a midline sternotomy with
subsequent dissection of the great vessels and the anterior surface of the
trachea. The patient was placed on cardiopulmonary bypass. Rigid videobronchoscopy
was then performed by the otolaryngology team to identify the superiormost
aspect of the stenosis. This was verified by passing a 25-gauge needle through
the midline of the anterior trachea. Under continued bronchoscopic guidance,
the trachea was then incised from superior to inferior so that the entire
stenosis was opened (Figure 2).
It is important that all complete rings are incised. The length of the stenosis
cannot be ascertained by external assessment of the trachea. The vertical
defect in the opened trachea was measured with a caliper and the graft fashioned
accordingly. If the graft was not long enough, a second piece of cartilage
was obtained through the initial harvest site. The graft was then sewn into
place using nonabsorbable monofilament sutures with the otolaryngologist closing
the left side of the defect and the cardiothoracic surgeon the right side.
This arrangement was technically efficient and saved time. The perichondrial
surface of the graft faced the lumen (Figure
3). Care was taken so that the graft did not prolapse into the lumen
of the trachea and so the sutures also remained extralumenal. None of the
sutures were tied until all had been placed. After they had been tied, the
position of the graft was verified by another bronchoscopy. The closure was
intended to be airtight and any leaks were identified by placing isotonic
sodium chloride solution in the wound and applying positive pressure ventilation.
Leaks were closed with further sutures. An appropriate-sized nasotracheal
tube was placed so that it did not fit snugly. Because CCT is a rigid reconstruction,
the nasotracheal tube did not serve as a primary stent and did not need to
pass distal to the repair site. The distal tip of the tube usually resided
near the midportion of the graft. Once adequate ventilation was obtained,
the patient was removed from cardiopulmonary bypass and both wound sites were
closed.
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Figure 2. The heart, great vessels, incised
trachea, and bypass cannulae are shown. The entire stenosis must be opened.
Illustration reprinted courtesy of Mosby Inc.22
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Figure 3. The graft is sewn into position
with the perichondrial surface facing the lumen of the trachea. The graft
and sutures must remain extralumenal. Illustration reprinted courtesy of Mosby
Inc.22
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Patients were sedated in the intensive care unit for 7 to 10 days. Specific
sedation regimens varied according to the preferences of the managing intensivist.
In general, patients received midazolam hydrochloride and fentanyl citrate.
An attempt was made to avoid prolonged complete paralysis, but when paralysis
was necessary, vecuronium bromide was used. Patients were returned to the
operating room for another bronchoscopy to check the status of the graft and
to remove any granulation tissue that may have formed. Formal extubation was
performed later in the intensive care unit after the patient had fully awakened.
Any further diagnostic or therapeutic bronchoscopies were performed on an
as-needed basis.
CHART REVIEW
A retrospective chart review of all patients admitted to St Louis Children's
Hospital from January 1986 to January 2000 with the diagnosis of CLSTS was
undertaken. All study subjects underwent CCT as the primary repair of their
tracheal disease. This procedure became the preferred technique for CLSTS
at St Louis Children's Hospital in 1986 and has been the primary repair technique
used since then. This report documents our entire experience with CCT.
The following patient data were extracted: date of birth; sex; race;
length of stenosis; minimal diameter of stenosis; associated anomalies; age
at tracheal repair; weight at repair; major postoperative complications; number
of postoperative days on ventilator; number of postoperative days until discharge
from the hospital; and number of postoperative bronchoscopies. Complications,
which were minor and did not affect the patient's management or course, were
not recorded.
This study was reviewed and approved by the Human Studies Committee
of Washington University School of Medicine, St Louis, and assigned approval
number 01-0151.
RESULTS
Ten patients were identified as having undergone CCT for CLSTS. There
were 8 males and 2 females. Seven of the patients were white and 3 were black.
Cumulated data are shown in Table
1 and Table 2. Age at
repair ranged from 1 to 56 weeks with an average age of approximately 18 weeks.
Weight at repair ranged from 3.1 kg to 9.9 kg with an average of 5.2 kg. Length
of tracheal stenosis ranged from 2.0 cm to 5.0 cm with an average of 3.2 cm.
Minimal diameter of stenosis ranged from 1.0 mm to 2.5 mm with an average
of 1.9 mm. Postoperative days receiving ventilator support ranged from 7 to
81 days with an average of 17 days and a median of 9.5 days. Postoperative
days until discharge ranged from 11 to 180 days with an average of 35.2 days
and a median of 17 days. Postoperative bronchoscopies (both diagnostic and
therapeutic) ranged from 1 to 139 with an average of approximately 18 and
a median of 4.5.
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Table 2. Postoperative Patient Data*
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Forty percent of the patients experienced major postoperative complications.
Seventy percent of the patients had other congenital anomalies and 40% were
cardiac in nature. Three of the children had syndromes (Down and VATER [vertebral,
anal, tracheal, esophageal, radial, and renal anomalies]).
No patient died from an inadequate trachea. Patient 6 died 1.8 years
after the tracheoplasty due to a cardiac event. Patient 9 died 16 days after
the repair because of left lung air trapping secondary to a stenotic left
mainstem bronchus along with a hypoplastic right lung. The intermediate survival
rate for the group was 90% and the long-term survival rate is 80%. Seven of
the 8 living patients are active and without tracheostomy. The average length
of time since surgery for the survivors is 8 years.
Patient 4 did well for 11 years after his tracheoplasty until he developed
stridor and dyspnea on exertion. Bronchoscopy showed a 3-cm soft stenosis
of the midtrachea. This was initially treated with balloon dilation, but eventually
required excision and end-to-end anastomosis of the tracheal ends. He is again
fully active.
Patient 5 has experienced a prolonged and very complicated course. His
data for postoperative days receiving ventilator support, postoperative days
until discharge, and postoperative bronchoscopies skew the group average for
these information items. Therefore, median group values are also given and
probably more accurately represent the group. Patient 5 developed distal tracheal
stenosis after his repair and required placement of a tracheostomy tube 1
month later. Recurring granulation tissue near the carina has required frequent
carbon dioxide laser treatments working through the stoma site to maintain
a functional airway. For 5 years the patient was physically active until he
experienced respiratory arrest at home resulting in anoxic encephalopathy.
He now exists in a vegetative state, yet continues to require laser treatments
to open his distal airway.
Patient 7 underwent CCT after a tracheostomy had been placed at an outside
hospital for CLSTS. One month after the repair, she developed focal stenosis
at the old tracheostomy site, which required placement of a second cartilage
graft. Her further course was uncomplicated.
COMMENT
Pediatric tracheal stenosis may be classified as acquired, extrinsic
congenital, or intrinsic congenital. Acquired lesions are usually secondary
to trauma, intubation, tracheostomy, ingestion, burn, or tumor. Extrinsic
congenital lesions are usually due to anomalies of the great vessels or mediastinal
or esophageal disease. Intrinsic congenital lesions include tracheal aplasia,
primary tracheomalacia, hamartomas, webs, and complete tracheal rings.
As described earlier, congenital tracheal stenosis due to complete rings
may be subclassified as generalized hypoplastic, funnel shaped, or segmental.2 If any of these malformations involve greater than
one half of the length of the trachea, it is considered CLSTS. Patients in
whom CLSTS causes less than 50% narrowing of the trachea may not be particularly
symptomatic and can usually be managed conservatively. It is thought that
the stenosis may "grow" with the child.4 Those
in whom CLSTS is responsible for greater than 50% narrowing of the trachea
will surely come to medical attention. To further complicate the management
of these patients is the fact that the majority will also have associated
congenital anomalies, particularly of the cardiovascular system.23 Pulmonary
artery sling and pulmonary hypoplasia are common associated anomalies. Our
series is unusual in that no vascular slings or rings were encountered. Three
of our patients were syndromic.
The timing and manner of presentation of children with CLSTS are variable.
The infant may have respiratory distress at birth. Others present with failure
to thrive, or initially do well until their growth outstrips their ability
to adequately ventilate. Some are incidentally found after a difficult intubation
for an unrelated surgery or after superimposition of an upper respiratory
tract infection. The majority of patients with CLSTS will present with biphasic
stridor and increased work of breathing.
Diagnosis begins with a high degree of suspicion. Plain films and airway
fluoroscopy may aid in the diagnosis, but can underestimate the extent of
disease. Contrast tracheography and bronchography are dangerous procedures
and no longer have a role. Computed tomography and magnetic resonance imaging
can be useful in the diagnosis of CLSTS and may further define potential vascular
anomalies. However, extreme caution should be used if sedation is necessary
to perform these studies. Angiography and echocardiography are warranted to
diagnose cardiovascular anomalies.
The gold standard for the diagnosis and evaluation of CLSTS is rigid
bronchoscopy under general anesthesia. The endoscopist must make an effort
to determine the width, length, and site of the stenosis. Filming the procedure
on videotape to review later with a cardiothoracic surgeon is recommended.
An attempt should also be made to document the status of vocal cord mobility.
Congenital tracheal stenosis involving less than 50% of the length of
the trachea may be treated by segmental resection. Longer stenoses will require
a different intervention and various options are discussed below. Also, a
variety of intraoperative airway management techniques are available. These
include endotracheal intubation, endotracheal jet ventilation, bronchoscopic
ventilation, extracorporeal membrane oxygenation, and distal (bronchial) ventilation.
We used the cardiopulmonary bypass technique in our series and found this
optimal. By removing the need for upper airway ventilation, the surgical field
is less encumbered and the surgery can proceed in an unhurried and steady
fashion.
The optimal repair technique for CLSTS is controversial. Costal cartilage
tracheoplasty was first described by Kimura et al in 1982.15 The
advantages of CCT include a graft material that is plentiful and autologous.
The cartilage provides a rigid reconstruction, which secondarily allows for
a relatively short period of postoperative intubation. Subsequently, the formation
of granulation tissue, though always a concern, may be less than that seen
with a technique such as pericardial patch. Because of graft rigidity, the
endotracheal tube need not be positioned near the carina, a site prone to
granulation tissue formation. Another advantage is that the cartilage graft
may be fashioned to extend over stenosis of a mainstem bronchus. Experimentally,
costal cartilage has been shown to epithelialize well24 and
this has been confirmed clinically with postoperative bronchoscopy. Disadvantages
of CCT include the existence of 2 wound sites (though the graft may be harvested
through the midline sternotomy) and that the initial graft may be too short
to encompass the entire stenosis. This latter issue may be addressed by harvesting
2 pieces of cartilage or by resecting a segment of trachea. Long-term growth
potential of the cartilage graft is also a concern. Oue et al25 report
histological findings of costal cartilage grafts from 6 patients who died
1 month to 2 years after CCT. They found that the graft gradually diminished
in size and was ultimately replaced completely by mature scar tissue. Nonetheless,
the diameter of the reconstructed trachea was not reduced. Other authors have
also noted that the grafts are replaced with scar, though with good functional
results.15, 19
The fact that patients 1, 2, and 3 are now more than 10 years out from
their procedures, without significant airway compromise, would seem to support
CCT as a procedure with the potential for long-term success. What truly constitutes
"long-term success" is somewhat arbitrary and it will be interesting to follow
these patients over the ensuing years. We are unsure as to the etiology of
the restenosis seen in patient 4, though are alert to the possibility that
it is secondary to complete degeneration of the graft. The poor outcome in
patient 5 is related to tracheomalacia and bronchomalacia, which were present
in addition to CLSTS and it is doubtful whether any other technique would
have been more successful. The death of patient 9 speaks to the worsened prognosis
for patients with CLSTS and associated pulmonary anomalies (left mainstem
bronchus stenosis, right lung hypoplasia, and hyaline membrane disease). Our
survival rate compares favorably with that of other authors.10-14,19
In addition to CCT, the other preferred technique for augmentation tracheoplasty
is the pericardial patch. This was first described by Idriss et al10 in 1984. With the patient on cardiopulmonary bypass,
a piece of pericardium is harvested through the midline sternotomy. It is
then sewn to the anterior tracheal defect and also tacked anteriorly to the
innominate artery. The repair is left stented by the endotracheal tube for
1 to 2 weeks. Advantages of this technique include a graft material that is
autologous, plentiful, and harvested from the same operative field as the
site of tracheoplasty. Disadvantages include the fact that this is not a rigid
reconstruction and, therefore, requires longer endotracheal tube stenting.
This may result in greater granulation tissue formation necessitating more
therapeutic bronchoscopies, particularly when the repair site extends to the
carina. Brown et al14 have shown that the pericardium
becomes epithelialized and later replaced with normal mucosal and submucosal
tissue. Spiral computed tomography scans in their long-term survivors document
continued growth of the trachea as the patients aged.
Slide tracheoplasty is another surgical technique for the treatment
of CLSTS. It was first described by Tsang et al26 in
1989 and later modified by Grillo.27 Several
other authors have documented its success.28-30 With
this technique, the trachea is divided transversely through the middle of
the stenosis. The tracheal ends are then spatulated by longitudinal incisions
on the anterior surface of one end and the posterior surface of the other
end. The tracheal ends are then advanced over each other and anastomosed.
The resulting repair reduces the length of the stenosis by one half and increases
the lumen of the trachea by a factor of 4. The advantages of this technique
include avoidance of a graft material and a rigid reconstruction. Postoperative
endotracheal stenting time is reduced or unnecessary. Less granulation tissue
is formed and fewer bronchoscopies are required. Disadvantages of this technique
include its potentially limited applicability for extremely long stenoses
and those which involve the carina or mainstem bronchi.14 It
may also be difficult to perform on very young patients. In fact, the cumulative
experience in young infants has been small.
Adult tracheal reconstruction with a cadaveric tracheal homograft was
first described by Herberhold et al31 in 1980.
The technique was first described in children in 1996 by Jacobs et al.32 Further reports have attested to its feasibility.33-34 With this technique, fixed cadaveric
trachea is sewn to an opened stenotic trachea. A temporary silicone stent
is placed in the lumen and endoscopically removed 10 to 12 weeks later. The
advantage of this technique is its ability to reconstruct very large tracheal
defects including stenoses of the mainstem bronchi. Disadvantages include
the availability of cadaveric trachea, granulation tissue formation secondary
to the stent, and growth concerns of the graft. The authors recommend this
technique only for those patients in whom other reconstruction approaches
have failed.
Backer et al35 recently reported a novel
technique for the treatment of CLSTS using a free tracheal autograft. With
this technique, the anterior trachea was vertically incised through the area
of stenosis and the midportion of the stenotic trachea was excised. The posterior
ends of the remaining trachea were anastomosed in end-to-end fashion. The
excised tracheal segment was then used as a free autograft to repair the anterior
tracheal defect. When the graft was not large enough to cover the entire defect,
a pericardial patch was added to the repair.
In the future, repair of CLSTS may involve the use of living allogeneic
tracheal tissue grown in a laboratory. Macchiarini et al36 have
reported growing embryonic human tracheas in the abdominal cavity of nude
mice. These tracheal segments were then used to reconstruct surgically induced
tracheal stenosis in piglets. The repairs were successful with and without
immunosuppression.
Less invasive techniques for the management of CLSTS include the use
of balloon dilation37-38 and the
placement of expandable metallic airway stents.39 The
former technique usually requires multiple applications and may better serve
as a bridging maneuver until definitive repair can be performed. The placement
of metal airway stents is considered a salvage technique in patients with
complications in whom earlier tracheoplasty has failed or who cannot tolerate
it.
As the above discussion indicates, there is no consensus on the optimal
repair technique for CLSTS. Costal cartilage tracheoplasty, pericardial patch,
and slide tracheoplasty seem to be preferred techniques.
CONCLUSIONS
We report our experience with CCT for all patients who presented with
CLSTS to St Louis Children's Hospital from 1986 to 2000. All of the repairs
were performed with an otolaryngologist working in conjunction with a cardiothoracic
surgeon and while the patient was on cardiopulmonary bypass. Most of the patients
were small infants, many with associated anomalies or syndromes. No patient
died of an inadequate tracheal airway, although one patient is tracheostomy
dependent. The survival rate for the group is 80% and 7 of the 10 patients
are now fully active without tracheostomy. We believe that CCT should be considered
a preferred technique for the management of CLSTS.
AUTHOR INFORMATION
Accepted for publication April 8, 2002.
This study was presented at the 16th Annual Meeting of the American
Society of Pediatric Otolaryngology, Scottsdale, Ariz, May 11, 2001.
Corresponding author and reprints: James W. Forsen, Jr, MD, Division
of Pediatric Otolaryngology, St Louis Children's Hospital, One Children's
Place, St Louis, MO 63110.
From the Division of Pediatric Otolaryngology (Drs Forsen and Lusk),
and the Department of Otolaryngology–Head and Neck Surgery, Division
of Cardiothoracic Surgery (Dr Huddleston), Department of Surgery, Washington
University School of Medicine and St Louis Children's Hospital, St Louis,
Mo.
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