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Tracheal agenesis: A case report and review
of the literature
JOSEPH KERSCHNER,MD, and DOUGLAS W. KLOTCH,MD, FACS,Tampa, Florida
Tracheal agenesis is a devastating congenital anomaly
first described in 1900 by Payne. 1 In 1962 Floyd et al.2
classified tracheal agenesis into three types (Figs. 1, 2,
and 3). One year later, Fonkalsrud et al. 3 attempted the
first surgical correction of this anomaly. This attempt,
as well as other interventions, have been unsuccessful
in allowing any long-term survival.
Eighty-seven cases have previously been identified
in the world literature. This additional Floyd type III
case typifies the problems of assessment and management of this fatal anomaly. A discussion of the embryology and associated congenital anomalies is presented.
The clinical aspects of managing this abnormality are
described along with previous attempts at surgical correction. Newer investigations may lead to a solution of
this lethal anomaly.
CASE REPORT
A full-term, 3300-gm girl was delivered by normal spontaneous vaginal delivery to a 23-year-old gravida 2, para 1
mother who had an uncomplicated pregnancy with a normalappearing ultrasound at 20 weeks. After delivery the child was
noted to have respiratory distress with Apgar scores of 3 and
6 at 1 and 5 minutes. The infant was noted to have an absent
cry. Attempt was made to intubate the infant without success.
Saturations were maintained with the use of bag-valve mask.
Attempts at intubation by the neonatology service were also
unsuccessful, and the child was taken to the neonatal intensive
care unit while being supported by bag and mask. The ototaryngology service was called, and after direct laryngoscopy
revealed no subglottic opening, the infant was taken directly
to the operating room. Further endoscopy at this time revealed
essentially normal-appearing vocal folds with complete
occlusion of the airway immediately in the subglottic area. A
patent esophagus was identified posteriorly. A neck exploration was performed in an attempt to identify a tracheal remFrom the Divisions of Otolaryngology(Dr. Kerschner) and Surgery
(Dr. Klotch), University of South Florida.
Reprint requests: Douglas W. Klotch, MD, Harbourside Medical
Towers, 4 Columbia Dr., Suite 730, Tampa, FL 33606.
Otolaryngol Head Neck Surg 1997;116:123-8.
Copyright © 1997 by the American Academy of OtolaryngologyHead and Neck SurgeryFoundation, Inc.
0194-5998/97/$5.00 + 0 23/4/72278
nant. Only the esophagus could be identified, and intubation
of this structure allowed mechanical ventilation with good
saturations. A presumed diagnosis of tracheal agenesis was
made, and contrast material was used to radiographicatly confirm this (Fig. 4). The child's situation was discussed with the
family, who elected no further intervention. The child was
returned to the neonatal unit and allowed to die. The family
refused a postmortem examination.
DISCUSSION
Tracheal agenesis is a devastating congenital anomaly that is made even more tragic when it presents in the
face of a seemingly normal pregnancy. The diagnosis is
now often made antemortem, but the surgeon still has
little to offer the child to significantly prolong life.
The terms tracheal agenesis, tracheal atresia, and
tracheal aplasia have each been used in the literature to
refer to essentially the same entity. 4-8 These terms have
also been used to differentiate more severe from less
severe cases. This fact and the occasional inclusion of
severe cases of tracheal stenosis have led to some confusion in the cataloging and reporting of this entity. We
evaluated the world literature in an attempt to identify
cases not previously included in other reviews. We
excluded cases that we believed were not clearly
defined examples of tracheal agenesis. Eighty-seven
cases of tracheal agenesis were identified in the world
literature (Table 1). Some confusion occurs in assigning
cases to the Floyd type I category. At presentation cases
of Floyd type I have a short segment of distal trachea
arising from the anterior esophagus, which then divides
into the main-stem bronchi (Fig. 1). Essentially any
degree of absent trachea with a concomitant tracheoesophageal communication could technically be classified as a type I tracheal agenesis. Other classification
schemes have attempted to further describe and include
these variations.33 The classification scheme of Faro et
al.33 divides tracheal agenesis into categories A through
G, with type A representing total pulmonary agenesis
and type G representing tracheal stenosis.
Although any pathologic entity will have some
degree of variability in severity, it is important to distinguish tracheal agenesis from severe cases of stenosis
or a short segment of tracheal atresia. These latter
123
OtolaryngologyH e a d a n d N e c k Surgery
124
Table
KERSCHNER a n d KLOTCH
J a n u a r y 1997
I. L i t e r a t u r e r e v i e w
Case
no.
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19, 20
21
22
23
24
25
26
27-30
31
32-36
37
38
39, 40
41
42
43
44
45
46
47, 48
49
50
51
52, 53
54
55
56
57, 58
59
60
61
62
63
64
65
66
67
68
69
70
Source
Payne ~
Beneke 9
Walched °
Fritz ~~
Benesova and Peter 12
MareM 3
Milles and Dorsey TM
Kessel and Smith 15
Sandison 16
Hempe117
Devenis and Otis I8
Onarir and Sariyalcin 19
Floyd et al. 2
Fonkalsrud et al. 3
Witzelben 7
McCraken et al 8
Devi and More 21
Stowens 2°
Lyons and Bruce 22
Colavecchio 23
Joshi 24
Elmer 25
McNie and PryseDavis 26
Peison et al. 6
Altman et al. 27
Hopkinson 28
Hong et al. 29
Effman et al. 3o
Warfel and Schulz 31
Perel et al. 32
Faro et al. 33
Morgan et al. 34
Donovan and Friedman 4
Anderson et al. 35
Buchino et al. 36
Siplovich and Cywes 37
Parameswaran et al. 3s
Haupt and Edwards 39
Paes et al. 4o
Reilly et al. 41
Solano-Larranga et al. 51
Milstein et al. 43
Evans et al. 44
Haskovcova 45
Sakal et al. 46
Holinger et al. 47
Kearns and Miller 4s
Diaz et al. 49
Bray and Lamb 5°
Brandenkamp et al. 51
Zimmermann et al. 53
Herbert et al. 54
Ruiz et al. 55
Scurry et al. 56
Rovira et al. 57
Ishii et al. 58
Nakada et al.59
Statz et al. 6o
T a b l e 1. L i t e r a t u r e r e v i e w - - c o n t ' d
Year
1900
1905
1928
1933
1934
1940
1950
1953
1955
1956
1957
1961
1962
1963
1963
1964
1966
1966
1968
1969
1969
1969
1970
1970
1972
1972
1974
1975
1976
1977
1979
1979
1979
1981
1982
1982
1983
1983
1984
1984
1984
1985
1985
1985
1986
1987
1987
1989
1988
1988
1988
1988
1988
1989
t989
1989
1989
1989
Floyd's
type
Case
no.
71
III
II
II
II
III
I, II
II
II
1
III
I
II
II, I, II, I
II
II, III, II, II, II
II
II
II, II
II
II
I
II
II
III
III, II
II
II
III
II, II
III
II
II
I1,$
II
I
III
II
II
II
III
I
III
II
III
III
Total type l, 11 (~13%); total type II, 53 (-62%); total type III, 22
(~26%).
*Case of total pulmonary agenesis with tracheal agenesis.
l-Type unclear from translation of article.
:t:Second case type not described.
72
73
74
75
76
77
78
79
80-84
85
86
87
88
Source
Year
Floyd's
type
ArizmendiDorantes et al. 61
Branger et al. 62
Brichard et al. 63
McDonald and Orio164
Chiu et al. 5
Dost et al. 65
Schiffmann et al. 66
Well 67
Lopaz et al. 68
Koltai and Quiney 6e
Rodriguez et al. 7o
Downing TM
Raso 72
Present case
1989
III
1989
1990
1990
1990
1991
1991
1991
1991
1992
1992
1992
1993
1993
II
II
III
III
II
II
II
II
II, III, I, I, II
III
III
II
Ill
examples have a significant portion of healthy trachea,
which may allow for survival by prompt surgical intervention. 73 They definitely represent a different clinical
entity and likely have a different embryologic genesis
as well. It is best to reserve the term tracheal agenesis
for cases with a very small, if any, segment of normal
distal trachea. These patients cannot be saved by tracheotomy or other surgical intervention at this time.
The trachea and esophagus begin their development
from the foregut during the third and fourth weeks of
gestation. However, the embryology of tracheal stenosis is an unresolved issue. Koltai and Quiney's review
of this subject is excellent,69 and they point to at least
three competing theories. Initially, most accepted the
theory from the works of His, 75 Bremer,76 and Smiths
This theory proposed the formation of a tracheoesophageal septum during development. Tracheal agenesis was presumed to result from ventral displacement of
this septum. Later work by Zaw-Tun78 and Kluth et al.79
called into question the tracheoesophageal septum.
Zaw-Tun claimed that the trachea developed as a ventral outgrowth of the foregut. Kluth et al. showed that
the esophagus and trachea develop as the foregut
decreases in size by infolding, without formation of a
fused septum.
The prenatal presentation of infants with tracheal
agenesis has ranged from high-risk, complicated pregnancies to completely uneventful ones. One significant
prenatal finding in a number of presentations is that
polyhydramnios.
After delivery, all infants display respiratory distress
as well as an absent or exceedingly weak cry. Attempts
at intubation will reveal an absent glottic or subglottic
opening and an inability to intubate the infant. Some
OtolaryngologyHead and Neck Surgery
Volume 116 Number 1
KERSCHNERand KLOTCH 125
,.;.:..,
Fig. 2. Type II tracheal agenesis as described by Floyd
et al. 2
Fig. 1. Type I tracheal agenesis as described by Floyd et al. 2
confusion may arise by esophageal intubation, which
generally allows relatively adequate ventilation in the
short term. Stabilization may also be achieved by bagvalve mask.
Further respiratory difficulty or suspicion of the
diagnosis generally leads to endoscopic evaluation of
the infant or emergent neck exploration to identify the
trachea and attempt a tracheotomy. Laryngoscopy,
bronchoscopy, and esophagoscopy often confirm the
diagnosis. Further information can be obtained by a
contrast study through the esophagus. Any doubt about
the child's anatomy should be confirmed with neck
exploration to ensure that a tracheal remnant for tracheostomy does not exist. 49,69
Further management of tracheal agenesis has yielded no long-term survival. Intubation of the esophagus
with either an endotracheal or tracheostomy tube provides a temporary airway. Gastric decompression must
also be performed to prevent gastric and intestinal dis-
tention from the use of the esophagus for ventilation. In
type I lesions the short distal tracheal segment may be
intubated directly.69
Several attempts have been made to achieve more
definitive repair. The first was made by Fonkalsrud et
al. in 1963.3 Their attempt involved division of the cervical esophagus. The proximal end provided drainage
of oral and pharyngeal secretions, and the distal end
was brought out as a stoma and intubated with a tracheostomy tube for ventilation. The chest was ~ e n
entered, and distal to the takeoff of the bronchi another
division of the esophagus was performed. This procedure allowed separation of the newly created pseudotrachea and the gastrointestinal tract. The distal portion
of the second division was used for enteral feedings.
Surprisingly, decannulation was apparently successful
several days after this procedure. Fonkalsrud's patient
survived for 6 weeks, the longest survival period to
date.
In 1972 Altman et al.27 used a procedure that varied
from Fonkalsrud's by performing a gastric division
126 KERSCHNERand KLOTCH
OtolaryngologyHead and Neck Surgery
January 1997
Fig. 4. X-ray to confirm diagnosis of tracheal agenesis.
Fig. 3. Type III tracheal agenesis as described by Floyd
et al. 2
instead of dividing the distal esophagus. This procedure
provided the theoretical advantage of not having to
enter the chest cavity. Other attempts have been made
since, using essentially the same principles, and without
any significant success.36,57,68
The attempts at surgical correction are hampered by
two major factors when the esophagus is used as a
pseudotrachea. The first difficulty is that the esophagus
lacks rigidity and is therefore prone to collapse with
normal inspiratory forces. Second, and more importantly, the esophagus lacks the ciliated respiratory epithelium of the normal trachea. This prevents the efficient
handling of secretions and inevitably results in pneumonia, the cause of death in Fonkalsrud's patient.
Further management of tracheal agenesis is also
complicated by the many other congenital anomalies
with which it is often associated. Several investigators
noted that cases of tracheal agenesis were frequently
accompanied by other defects. 3°,35,4~,43 In 1981
Anderson et al. 35 suggested that tracheal agenesis might
be linked to the VATER association. Quan and
Smiths0,81 had first proposed the VATER association in
1972. This association included vertebral defects, and
atresia, tracheoesophageal fistula and esophageal atresia, radial dysplasia, and renal defects. It was later
expanded to VACTERL to include cardiac and limb
defects.69.82 Reilly et al.41 and Milstein et al. 43 provided
reviews that supported the link between tracheal agenesis and the VATER association. Further investigation by
Evans et al. 44 suggested that tracheal agenesis best fit
into a new association. This was later termed the
TACRD association, and included tracheal agenesis or
(laryngo)tracheal atresia, cardiac anomalies, radial ray
defects, and duodenal atresia. 44,49How tracheal agenesis is linked to these other nonrandom deformities has
yet to be elucidated. Whichever association best
includes tracheal agenesis, it is important to realize that
any future attempts at dealing with this anomaly will
often have other pathologic conditions to address as
well.
A number of investigators have looked at possible
solutions for various tracheal anomalies. Most of the
investigations have centered around solving the more
common problem of severe or recurrent tracheal stenosis. Various prosthetic materials have been proposed,
including Marlex, Dacron, and Silastic,83-85 Both pedicled and free flaps, primarily consisting of periosteal
designs, have also been proposed.86-90 Any solution
involving replacement of a large portion of the trachea
obviously becomes that much more difficult. These
potential solutions are plagued with difficulties similar
OtolaryngologyHead and Neck Surgery
Volume 116 Number I
to the use o f the e s o p h a g u s as a trachea. R e c o n s t r u c t i o n
m u s t c o n t e n d w i t h the a b s e n c e or i n c o r p o r a t i o n o f resp i r a t o r y e p i t h e l i u m . T h e a i r w a y m u s t b e sufficiently
r i g i d to p r e v e n t c o l l a p s e w i t h i n s p i r a t o r y forces a n d
m u s t also a d a p t w i t h g r o w t h o f the child. T h e r e is also
the difficulty o f g r a n u l a t i o n tissue a n d s t e n o s i s o c c u r r i n g at the suture line o f a n y i n c o r p o r a t e d graft. In 1992
C h o p r a et al.Ss w e r e able to g r o w r e s p i r a t o r y e p i t h e l i u m
o n p r o s t h e t i c D a c r o n b y cell culture t e c h n i q u e s . S u c h
w o r k will p e r h a p s l e a d to a b e t t e r u n d e r s t a n d i n g o f resp i r a t o r y e p i t h e l i u m a n d a m e t h o d to e f f e c t i v e l y incorp o r a t e it into r e c o n s t r u c t i v e m o d e l s . In addition, r e c e n t
a d v a n c e s i n t i s s u e m o l d i n g w i t h m i c r o v a s c u l a r free tissue a n d b o n e i n d u c t i o n m a y h o l d a s o l u t i o n to r e c o n s t r u c t i o n o f l o n g - s e g m e n t t r a c h e a l defects.9~
In s u m m a r y , t r a c h e a l a g e n e s i s is a rare b u t devastating a n o m a l y o f t e n f o u n d i n a s s o c i a t i o n w i t h o t h e r c o n g e n i t a l defects. P r o m p t i n t e r v e n t i o n o f t e n allows for
p r e m o r t e m d i a g n o s i s . It is i m p o r t a n t t h a t a n a c c u r a t e
d i a g n o s i s b e m a d e a n d t h a t less severe d i s e a s e b e r u l e d
out. A l t h o u g h several surgical a t t e m p t s h a v e b e e n m a d e
to p r o v i d e a n airway, n o l o n g - t e r m s u c c e s s h a s b e e n
a c h i e v e d . It is h o p e d that f u r t h e r i n v e s t i g a t i o n s in trac h e a l r e c o n s t r u c t i o n a n d t r a c h e a l p r o s t h e t i c s will e v e n tually a l l o w t h e s e i n f a n t s a c h a n c e at survival.
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