Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 15

Sugerman HJ: Gastric bypass surgery for severe obesity.

Semin Laparosc Surg 2002;9:79-


85.
Sugerman HJ, Sugerman EL, DeMaria EJ, et al: Bariatric surgery for severely obese
adolescents. J Gastrointest Surg 2003;7:102-108.
Surgeons, American College of: Recommendations for Facilities Performing Bariatric
Surgery. Bulletin of the American College of Surgeons, No. 85, 2000.
Surgery, American Society for Bariatric: Guidelines for Bariatric Surgery. Bulletin of the
American College of Surgeons, No. 85, 2000.
Taranger J, Engstrom I, Lichenstein H, Svennberg- Redegren I: Somatic pubertal
development. Acta Paediatr Scand Supp! 1976;258(Suppl):121-135.
Ten S, Maclaren N: Insulin resistance syndrome in children. J Clin Endocrinol Metab
2004;89:2526-2539.
Thompson SM, Dahlquist LM, Koenning GM, Bartholomew LK: Brief report: Adherence-
facilitating behaviors of a multidisciplinary pediatric rheumatology staff. J Pediatr Psychol
1995;20:291-297.
Tounian P, Aggoun Y, Dubern B, et al: Presence of increased stiffness of the common carotid
artery and endothelial dysfunction in severely obese children: A prospective study. Lancet
2001;358:1400-1404.
Towbin A, Inge TH, Garcia VF, et al: Beriberi after gastric bypass surgery in adolescence. J
Pediatr 2004;145:263-267. Turner RC, Cull CA, Frighi V, Holman RR, and for the UK
Prospective Diabetes Study Group: Glycemic control with diet, sulfonylurea, metformin, or
insulin in patients with type 2 diabetes mellitus: Progressive requirement for multiple
therapies (UKPDS 49). JAMA 1999;281: 2005-2012.
Van Itallie TB: Health implications of overweight and obe- sity in the United States. Ann
Intern Med 1985;103:983-988. von Mutius E, Schwartz J, Neas LM, et al: Relation of body
mass index to asthma and atopy in children: The National Health and Nutrition
Examination Study HI. Thorax 2001; 56:835-838.
Wahlqvist ML: Chronic disease prevention: A life-cycle approach which takes account of the
environmental impact and opportunities of food, nutrition and public health policies—the
rationale for an eco-nutritional disease nomenclature. Asia Pac J Clin Nutr 2002;11(Suppl
9): S759-S762.
Wang G, Dietz WH: Economic burden of obesity in youths aged 6 to 17 years: 1979-1999.
Pediatrics 2002;109:E81.
CHAPTER 78 _ Bariatric Surgery in Adolescents 1259
Wang Y: Is obesity associated with early sexual maturation? A comparison of the
association in American boys versus girls. Pediatrics 2002;110:903-910.
Wattigney WA, Srinivasan SR, Chen W, et al: Secular trend of earlier onset of menarche with
increasing obesity in black and white girls: The Bogalusa Heart Study. Ethn Dis 1999;9:181-
189.
Weisberg SP, McCann D, Desai M, et al: Obesity is associated with macrophage
accumulation in adipose tissue. J Clin Invest 2003;112:1796-1808.
Weiss R, Dziura J, Burgert TS, et al: Obesity and the meta- bolic syndrome in children and
adolescents. N Engl J Med 2004;350:2362-2374.
Wellen KE, Hotamisligil GS: Obesity-induced inflammatory changes in adipose tissue. J Clin
Invest 2003;112:1785-1788. Whitaker RC: Understanding the complex journey to obe- sity
in early adulthood. Ann Intern Med 2002;136:923-925. Whitaker RC, Deeks CM, Baughcum
AE, Specker BL: The relationship of childhood adiposity to parent body mass index and
eating behavior. Obes Res 2000;8:234-240. Whitaker RC, Wright JA, Pepe MS, et al:
Predicting obe- sity in young adulthood from childhood and parental obesity. N Engl J] Med
1997;337:869-873.
Wing YK, Hui SH, Pak WM, et al: A controlled study of sleep related disordered breathing in
obese children. Arch Dis Child 2003;88:1043-1047.
Wittgrove AC, Jester L, Wittgrove P, Clark GW: Pregnancy following gastric bypass for
morbid obesity. Obes Surg 1998;8:46 1-464; discussion 465-466.
Wysocki T, Greco P, Harris MA, et al: Behavior therapy for families of adolescents with
diabetes: Maintenance of treatment effects. Diabetes Care 2001;24:441-446.
Xu H, Barnes GT, Yang Q, et al: Chronic inflammation in fat plays a crucial role in the
development of obesity-related insulin resistance. J Clin Invest 2003;112:1821-1830.
Yajnik C: Interactions of perturbations in intrauterine growth and growth during childhood
on the risk of adult- onset disease. Proc Nutr Soc 2000;59:257-265.
Yarnell JW, McCrum EE, Patterson CC, et al: Prevalence and awareness of excess weight in
13- and 14-year-olds in Northern Ireland using recent international guidelines. Acta
Paediatr 2001;90:1435-1439.
Young-Hyman D, Schlundt DG, Herman L, et al: Evaluation of the insulin resistance
syndrome in 5- to 10-year-old overweight/obese African-American children. Diabetes Care
2001;24:1359-1364.
Duodenal Atresia and Stenosis— Annular Pancreas
Harry Applebaum, Steven L. Lee, and Devin P Puapong
The duodenum is the most common site of neonatal intestinal obstruction, accounting for
nearly half of all cases.'6 Although duodenal atresia, stenosis, and annular pancreas were
recognized as disease entities as early as the 18th century, successful treatment of
congenital high intestinal obstruction was a rare exception well into the 20th century. The
first reported case of duodenal atresia is attributed to Calder, in 1733.12 Cordes, in
1901,15 described the typical clinical findings associated with this congenital defect,
whereas Vidal from France and Ernst from the Netherlands are credited with the first
success- ful surgical repairs, in 1905 and 1914, respectively.244 By 1929, Kaldor was able to
identify 250 patients with duodenal atresia reported in the literature, although a review by
Webb and Wangensteen, in 1931, revealed only nine survivors.!® In stark contrast, modern
surgical management has resulted in greater than 95% survival, with the uncommon
mortalities usually related to anom- alies of other organ systems.*°
Historically, when duodenal atresia was encountered in association with trisomy 21 (Down
syndrome), a find- ing in nearly one third of patients, the newborn obstruc- tion was often
intentionally left untreated. It was not until the1970s that changing societal and medical
ethics led to a universal operative approach for infants born with these paired
anomalies.>®982 A gradual decline in the incidence of newborns with duodenal
obstruction can be attributed to the increasing ability of perinatolo- gists to determine an
abnormal chromosome association early in gestation, leading to elective termination of
many of these pregnancies. !4.67,76.83
‘The incidence of duodenal atresia has been estimated at 1 in 6000 to 1 in 10,000 births.?®
A recent large review of 18 congenital anomaly registries across Europe identified 64 cases
among 670,093 births, or 1 in 10,500.%° Although no specific genetic abnormality is
known to cause duodenal atresia, the number of reports of the anomaly occurring among
siblings and among several generations of a family, as well as its frequent
association with trisomy 21, suggests that one may be present.!3.29.37.53,57,59,71,83.90
1260
EMBRYOLOGY
During the third week of embryonic development, gastrulation occurs. The cellular surface
of the embryo facing the yolk sac becomes the endoderm, that facing the amniotic sac
becomes the ectoderm, while the mid- dle layer becomes the mesoderm. The endoderm
gives rise to the gut tube beginning in the fourth week of development. In the sixth week,
the gut epithelium proliferates rapidly, resulting in obliteration of the intes- tinal lumen.
The intestine is then gradually recanalized over the next several weeks of development.
Errors in recanalization are thought to be the primary cause of duodenal atresia and
stenosis. A total failure of recanal- ization leads to an atresia, whereas a partial failure leads
to a stenotic perforate membrane.®6.74 This etiology differs from that of intestinal
atresias and stenoses in other parts of the bowel, which are thought to result from vascular
accidents during the later phases of gestation.52
The pancreas begins to develop from the endodermal lining of the duodenum in the fourth
week of gestation. ‘Two pouches are formed that develop into a larger dorsal and a smaller
ventral pancreatic primordium. The ventral bud then rotates dorsally to fuse with the
dorsal bud during the eighth week. If the ventral bud fails to rotate completely, it remains
anterior to the duodenum and fusion with the ventral pancreatic primordium results in a
ring of pancre- atic tissue encircling the duodenum.§42:62.66,74
Approximately half of all infants with duodenal atresia or stenosis will also have a
congenital anomaly of another organ system.57-44,65,70,8087,91 Sweed collated statistics
for associated anomalies from a dozen large series of duode- nal obstructions and found
Down syndrome, annular pancreas, congenital heart disease, and malrotation to be the
most common (Table 79-1).8!
SPECTRUM OF INVOLVED DISORDERS
Several varieties of intrinsic and extrinsic congenital lesions can cause complete (81%) or
partial (19%) obstruction CHAPTER 79
TABLE 79-1 Associated Anomalies
(Collected Statistics)
Anomaly %
Down syndrome 28.2 Annular pancreas : 23.1 Congenital heart disease 22.6 Malrotation
19.7 Esophageal atresia/tracheoesophageal fistula 8.5 Genitourinary 8.0 Anorectal 4.4
Other bowel atresia 3.5 Other 10.9 None 45.0
Data from Sweed Y: Duodenal obstruction. In Puri P (ed): Newbom Surgery, 2nd ed,
London, Arnold, 2003, p 423.
of the duodenum.!® The spectrum of abnormalities causing intrinsic obstruction includes
imperforate and perforate webs of variable thickness within continuous bowel as well as
complete or almost complete bowel discontinuity. Abnormalities causing extrinsic obstruc-
tion include annular pancreas, preduodenal portal vein, Ladd’s bands, and volvulus.3759-
48,50,51,54,55,60
Gray and Skandalakis have grouped the variations of duodenal atresia into three types**:
Type 1 (92% of cases)?5: There is an obstructing septum (web) formed from mucosa and
submucosa with no defect in the muscularis. The mesentery is intact. A variant of type 1
duodenal atresia, a “windsock deformity,” can occur if the membrane is thin and elongated
(Fig. 79-1A). The base of the membrane usually lies in the second portion of the duodenum
but balloons out distally, distending the third and fourth portions. Thus, externally the
obstruction appears considerably more distal than it actually is.”
1261
Duodenal Atresia and Stenosis—Annular Pancreas
Type 2 (1% of cases): A short fibrous cord connects the two blind ends of the duodenum.
The mesentery is intact (see Fig. 79-1B).
Type 3 (7% of cases): There is no connection between the two blind ends of the duodenum.
There is a V-shaped mesenteric defect (see Fig. 79-1C).
In type | atresia the obstructing septum may vary in thickness from one to several
millimeters. Imperforate septa cause a complete obstruction, whereas those with central
perforations cause incomplete obstruction. With perforate septa, the diameter of the
opening directly determines the degree of obstruction and is there- fore inversely related
to the level of symptomatology (Fig. 79-2) .75
Although intrinsic blockage may occur in almost any portion of the duodenum, it occurs
near the juncture of the first and second portions in 85% of cases. The distal portion of the
common bile duct often traverses the medial portion of the septum, with the ampulla
commonly located on the proximal surface of the obstruction. In rare instances, the distal
portion of the duct is bifid, with proximal and distal openings, giving rise to what at first
glance appears to be an impossible situation of air and bile distal to a complete congenital
obstruction.?:!9
With an annular pancreas, the ring of pancreatic tissue encircling the duodenum may itself
cause an extrinsic partial obstruction. More often, however, a duo- denal atresia or stenotic
web underlies the annulus and is the actual cause of blockage.?? The pancreatic ductal
anatomy is altered, with major ductal structures travers- ing the annular portion (Fig. 79-
3). The distal duct is often located within the tissue of the underlying intrinsic obstruction,
and the ampulla opens onto its surface. In cases where there is no associated intrinsic
obstruction, the distal ductal anatomy is normal, and it is not uncom- mon to make a
diagnosis of annular pancreas much later in life during laparotomy for an unrelated
condition.*?
4z
atic Ate A, Type I duodenal atresia. B, Type II duodenal atresia. C, Type III duodenal atresia.
1262 PART VII
ABDOMEN
Figure 79-2 | ‘Typical duodenal web with central perforation.
A preduodenal portal vein crosses the anterior surface of the second portion of the
duodenum rather than running posterior to it and may cause incomplete obstruction by
compression. This rare cause of extrinsic duodenal compression is usually found in infants
with complex congenital heart disease .33.50
Intestinal malrotation results in Ladd’s bands that usually give rise to an extrinsic partial
obstruction of the second to third portion of the duodenum. Varying degrees of midgut
volvulus—acute, intermittent, or chronic—can occur in these infants, also resulting in
obstruction.’
CLINICAL PRESENTATION
Advances in prenatal care have allowed the majority of duodenal obstructions, both
complete and incomplete, to be detected before birth.5° Maternal polyhydramnios, noted in
30% to 65% of cases, is an early clue that should lead to further investigation.!655 Because
polyhydramnios often leads to preterm labor, approximately one half of
eee Annular pancreas with underlying web causing
partial duodenal obstruction.
a ieee Fetal ultrasound showing “double-bubble” sign.
these infants will be premature. The classic “double bubble” obstructive pattern is usually
easily identifiable on fetal ultrasound. The larger of the twin bubbles juxta- posed in the
fetal abdomen is the dilated, fluid-filled stomach, whereas the other is the distended
proximal duodenum (Fig. 79-4). This study will also occasionally identify an annular
pancreas.§388
Repeated bilious emesis is the characteristic clinical fea- ture of almost all newborns with
duodenal obstruction. Because of the proximal level of intestinal blockage, the infant does
not appear distended, although a subtle upper abdominal fullness may be noted. Placement
of a naso- gastric tube with a return of greater than 30 mL of fluid is suggestive of an
intestinal obstruction. In cases lacking prenatal diagnosis, it is somewhat common for an
incor- rect initial diagnosis of meconium aspiration to be made. During post-delivery
airway suctioning, the tracheal catheter may be inadvertently passed down the esopha-
gus, leading to wrongful interpretation of bilious gastric fluid as tracheal aspirate.
In patients with complete or high-grade duodenal obstruction, a plain radiograph of the
abdomen will generally confirm the diagnosis, with a finding of the “double bubble” sign.
The lack of more distal intestinal gas is diagnostic of a complete obstruction, whereas the
presence of gas indicates a partial obstruction. In situa- tions in which the diagnosis is
suspected but the “double bubble” sign is not clearly visible, injection of 30 to 60 mL of air
through the nasogastric tube may unmask this characteristic imaging finding (Fig. 79-5).
The recognition of partial obstructions may be considerably delayed if the obstruction is of
a relatively minor degree.?8 In this situation it is not uncommon for symptoms to first
occur when advancing the infant from formula to solid food, or it may be unmasked much
later in infancy, childhood, or, in rare instances, adulthood, when a progressive decrease in
motility or impaction of food or a foreign body causes more pronounced
symptomatology.27.56.68
With characteristic findings of duodenal obstruction on plain abdominal radiographs, it is
appropriate to proceed CHAPTER 79
gC tic-@weseeom Plain abdominal film of newborn with duodenal stenosis (perforated
web). Note small amount of air distal to “double bubble.” Same finding with lack of distal
air would indicate duodenal atresia.
directly to operative intervention without obtaining contrast studies. Occasionally, an
upper gastrointestinal contrast study may be helpful in differentiating intrinsic duodenal
obstruction from midgut volvulus. With intrin- sic obstruction, a smooth, rounded end will
usually be seen at the level of obstruction in the second portion of the duodenum and a
ligament of Treitz may be visible if the obstruction is incomplete (Fig. 79-6). A distal
“beaking” effect in the third portion should arouse concern about volvulus and the need for
an urgent operation. However, preoperative differentiation of the two anatomic problems
is completely unnecessary if the patient is to undergo exploration within a short period of
time.*6
The upper gastrointestinal contrast study is useful for the evaluation of older infants and
children with symptoms of chronic partial obstruction.'! Gastroduodenoscopy may be a
helpful diagnostic and sometimes therapeutic tool in these patients.*64
TREATMENT
Neonates with duodenal obstruction are initially man- aged with nasogastric or orogastric
tube decompression and intravenous fluids. Gastrointestinal losses are replaced
appropriately, and placement of a peripherally inserted central catheter line for parenteral
nutrition is recom- mended, because feeding is commonly delayed for up to several weeks
after repair. Assuming that a diagnosis of
1263
Duodenal Atresia and Stenosis—Annular Pancreas
aC see Duodenal atresia evident on upper gastrointestinal radiographic contrast study.
midgut volvulus has been reasonably excluded, surgical correction of duodenal obstruction
is not urgent. It can take place once the infant is optimized hemodynamically and
associated anomalies have been appropriately studied.** Pulmonary status and size may
preclude early operative intervention in very premature infants, and decompression
accompanied by parenteral nutrition may be required for several weeks before
undertaking repair.
The operation is best accomplished through a right upper quadrant transverse incision
halfway between the liver edge and the umbilicus, carried slightly across the midline. After
abdominal exploration, the right colon and hepatic flexure are then mobilized medially to
allow full exposure of the proximal duodenum. Eviscerating and positioning the small
bowel and colon cephalad and to the left of the incision best achieves access to the third
and fourth portions of the duodenum. This maneuver will fully expose the root of the
mesentery and ligament of Treitz. Although many patients with high-grade duo- denal
obstruction will have accompanying malrotation, on closer inspection a number will
actually be found to have a pseudo-malrotation, because the underlying grossly dilated
duodenum may cause abnormal leftward displace- ment of the right colon and hepatic
flexure. Absence of the ligament of Treitz will be noted in patients with true malrotation.
The entire duodenum is inspected and the probable location and type of the obstruction
noted. In a complete or nearly complete obstruction, the proximal duodenum appears as a
large, boggy, thickened sphere. In type I cases, diminutive, gasless bowel distal to this point
indi- cates that the obstruction is complete. In type II and III cases, the discontinuity of the
bowel will become evident during dissection. In patients with annular pancreas, 1264
PART VII Appomen
aC igceAeta Lapering of distended proximal duodenum over dilator.
pancreatic tissue will be seen extending circumferentially around the second portion of the
duodenum.
When there is gross dilatation of the proximal segment, a tapering duodenoplasty as the
initial part of the proce- dure may hasten the postoperative return of effective
peristalsis.!3,!9.38.46,77,92 This is accomplished by either suture plication or by resection
using a GIA stapler or needle-tip electrocautery and suture closure. The taper- ing is
positioned on the anterior or anterolateral surface to avoid damage to the common bile
duct, pancreas, and ampulla (Fig. 79-7).4° Additionally, division of the ligament of Treitz to
help mobilize the distal segment may greatly facilitate an eventual untwisted, tension-free
anastomosis.
When there is continuity of the proximal and distal duodenum, it is best to open the distal
bowel near the apparent point of obstruction, in a position and direc- tion suitable for a
potential bypass. If filmy or thin webs are identified as the cause of the obstruction, they
may sometimes be excised rather than bypassed. In this case, the incision is carried over
the web into the proximal lumen and the web is excised with cautery. If the ampulla is on
the medial aspect of the web, or is not well visualized, excision should include only the
lateral portion of the web. The duodenum is closed as a duodenoplasty in a transverse
manner, to shorten and widen the bowel over- lying the resection to minimize the risk of
stenosis. Web excision should only be attempted when the web is thin and when it is
clearly the only cause of obstruction.
In almost all situations, a duodenoduodenostomy, joining the bowel just proximal and
distal to the obstruc- tion, is the best corrective option. It is the most direct, physiologic
repair and, of the available options, has the least potential for later complications. When
this proce- dure is difficult because of patient anatomy, particularly in some small,
premature infants, duodenojejunostomy is an alternative choice. A loop of proximal
jejunum is chosen that will comfortably reach the proximal duo- denal segment and is
brought through the mesentery of the right transverse colon in a retrocolic position.
y wh
A LY
ak LEA Duodenojejunostomy.
Duodenojejunostomy provides postoperative results that are generally equivalent to those
obtained with duo- denoduodenostomy (Fig. 79-8). Gastrojejunostomy is associated with
frequent late complications of marginal ulceration and blind loop syndrome, and _
therefore should be avoided.
In recent series of patients with duodenal obstruction, duodenoduodenostomy has been
the procedure of choice in the great majority of patients (>80%), with duodeno-
jejunostomy used in approximately 10% and web excision in 5% to 10%.
Gastrojejunostomy was a rarely chosen option. 8:16.25,34
When performing a bypass anastomosis, a “diamond anastomosis” (proximal transverse
and distal longitudinal incisions) (Fig. 79-9A), first described by Kimura, is pre- ferred over
the “simple anastomosis” (proximal and distal longitudinal incisions) (see Fig. 79-9B) .4°-
+7.86 There is evidence that this asymmetrical anastomosis will maintain itself in a more
wide-open position and permit earlier transit of duodenal contents.
The antimesenteric incisions in each segment should be 1 to 2 cm in length, depending on
the size of the patient, to ensure an adequately patent anastomosis. With type III
deformities, the end of the distal segment is spatulated appropriately. Before making the
incision in the distal segment, it is useful to inject saline into the lumen while occluding the
bowel distally to slightly stretch the wall, thus enabling a technically easier anastomosis.
Additionally, a 10 French Foley catheter should be passed proximally into the stomach and
distally into the jejunum and pulled back with the balloon inflated, to ensure that no
additional web or a windsock deformity is overlooked. Before starting the anastomosis,
small ribbon retractors CHAPTER
cicw@we am A, “Diamond” anastomosis. B, “Simple” anastomosis.
can be placed in the proximal dilated segment to inspect the point of obstruction and to
determine the position of the ampulla of Vater. This anatomic landmark is usually easily
visible, even in small premature infants. In most patients, it is found in the proximal
segment, adjacent to or on the anteromedial aspect of the stenosis or web. In the remaining
patients, it will empty into the distal segment, also adjacent to or on the obstruction.
Figure 79-10 Bim Giivctomes
distal dilated duodenum after division of the ligament of Treitz. B, Onlay
of normal jejunum after resection
of distal duodenum (note: oblique resection to preserve ampulla).
79 1265
Duodenal Atresia and Stenosis—Annular Pancreas
The diamond anastomosis is constructed by placing initial stay sutures joining the
midpoints of each incision to the ends of the other. Placement should anticipate a posterior
row of knots inside the lumen and an anterior row on the outside. The posterior row of the
anastomo- sis is constructed using a repeating bisecting technique, to ensure even
placement of the sutures and good coaptation of the bowel edges. The anterior row of the
anastomosis is then completed in a similar fashion. The anastomosis is checked for patency,
and the intestine is returned to the abdominal cavity in its usual position. If the right colon
has been extensively mobilized and the ligament of Treitz taken down, or if a malrotation is
pres- ent, the intestine is replaced with the small bowel on the right and the colon on the
left, in the manner of a Ladd’s procedure. A nasogastric tube is positioned in the stom- ach.
Although commonly used in the past, gastrostomy tubes are now considered useful only in
selected infants who are not expected to feed orally in the near future. Some surgeons
routinely position transanastomotic feed- ing tubes, although their benefit has not been
clearly delineated.+6
Congenital obstruction of the distal duodenum at or near the ligament of Treitz presents an
especially difficult problem. The long segment of atonic dilated duodenum is difficult to
effectively taper, so that the reconstructed bowel and anastomosis are likely to function
poorly for a lengthy time period or not at all. In this situation, subtotal removal of the
dilated duodenum with preserva- tion of the ampulla is recommended (Fig. 79-10A).?34
The anterior wall of the second portion of the duodenum is opened and the ampulla of
Vater is located. The liga- ment of Treitz is taken down and the dilated duodenum is
dissected from the pancreas in a retrograde fashion to just distal to the ampulla. The first
and second portions of the duodenum are then tapered to near the level of
1266 PART VII AsBDdomMEN
the ampulla, with the resected proximal duodenum removed in continuity with the distal
duodenum. The end of the normal jejunum distal to the obstruction is spatulated and
anastomosed to the tapered proximal segment (see Fig. 79-10B).
When annular pancreas is encountered in association with duodenal obstruction, bypass is
always the procedure of choice. The ring of pancreatic tissue should never be transected
because of the major ductal structures that traverse it. Damage to these structures will lead
to leak- age of pancreatic fluid and/or pancreatitis. An obstruct- ing preduodenal portal
vein is bypassed in a similar manner.
There have been several recent reports of successful laparoscopic bypass procedures to
correct neonatal duodenal obstruction.§31,79 It is currently impossible to compare the
long-term outcomes of this technique with those of the classic open approach, because of
the lim- ited number of selected patients who have undergone this treatment.
Postoperatively, total parenteral nutrition is continued and nasogastric tube output is
monitored. As with other neonatal intestinal procedures, feedings may be started when the
volume of the nasogastric output has dimin- ished and its color has lightened and it
becomes clear. This stage is commonly reached within several days to a week but may be
prolonged. Small feedings are then initiated, with volume and concentration advanced as
tolerated. This is a rapid process in most infants, and the majority may be discharged
within one to several weeks.
COMPLICATIONS
Intraoperative
There are several intraoperative judgmental and techni- cal pitfalls that will lead to
postoperative difficulties.!7 Incorrect identification of the site of obstruction most
commonly occurs when a long, floppy web (windsock deformity) is present. The proximally
based web fills with gastrointestinal secretions and balloons out into the distal duodenum,
distending it and causing the site of obstruction to appear much more distal than it actually
is. The unwary surgeon, not recognizing the true attachment of the web, may then
construct a bypass anastomosis entirely distal to it. Additionally, on rare occasions, there
will be more than one obstruction present. A distal web is easily missed because of the lack
of any obvious adjacent proximal dilatation. The careful passage and withdrawal of balloon
catheters both proximally into the stomach and distally into the jejunum before starting an
anastomosis should prevent both of these situations,.2!,72
Postoperative
Prolonged feeding intolerance is the most common com- plication after surgery to relieve
duodenal obstruction. There is a great deal of variability in the time required for a bypass
anastomosis or web excision to function adequately. Although a variety of prokinetic
agents have
been proposed to hasten this process, none has been found to be of any consistent benefit.
In general, if no specific difficulties were encountered at the initial pro- cedure, there
should be concern if relatively normal function has not been achieved by 2 to 3 weeks. At
that time, an upper gastrointestinal series is helpful to search for residual anatomic
obstruction, anastomotic stenosis, previously unrecognized obstruction at a different
location, or poor peristalsis. Placing small clips on the anastomosis during initial surgery
will assist in determin- ing the location and cause of any residual problems. Any decisions
as to further surgical procedures should be based on a combined assessment of both
imaging studies and clinical gastrointestinal function. Dilated proximal duodenum may be
visualized radiographically for at least several months in the presence of a fully functional
bypass anastomosis.78
If prolonged poor function should occur, the finding of an anatomic obstruction is far less
likely than iden- tifying persistently poor peristalsis. Additional simple tapering of the
proximal duodenum may suffice to provide adequate additional motility, while subtotal
duodenectomy combined with proximal tapering is advisable if the initial obstruction was
in the distal duo- denum.*® Once adequate gastrointestinal function has been achieved,
further problems may develop but are uncommon.
Late duodenal obstruction may occasionally be noted in older infants and children. This
may occur after a seemingly successful neonatal bypass procedure or excision of web or de
novo when a diagnosis of partial duodenal obstruction was initially missed. In the former, a
piece of fibrous food or a foreign body may become impacted at the site of a partially
resected web or rela- tively narrow anastomosis that was either constructed to an
inadequate size, has become strictured over time, or has failed to grow with the child. In
the last instance, it may occur at the site of a relatively low-grade stenosis that has become
progressively symptomatic because of the development of proximal dilatation and
ineffective peristalsis. In others, no persistent anatomic obstruction can be demonstrated
after initial surgical correction but poor peristalsis can be demonstrated in an area of per-
sistent, and sometimes increasing, dilatation.!8
Proximal tapering is often very helpful at this time, either in conjunction with correction of
an obviously inadequate initial procedure or often by itself, in situations in which no
distinct anatomic narrowing is found.22!
Most of these older infants and children are large enough for full-function upper
gastrointestinal endoscopy, which may aid in the diagnosis and may be therapeutic by
permitting dilatation of anastomotic strictures or resection of webs.*9.64
OUTCOMES
Survival of infants with duodenal obstruction has increased from 45% to 95% over the past
half century.2%32.61.89 This dramatic improvement is primarily related to improved
diagnosis and surgical and postoperative management, although selective pregnancy
termination has likely played CHAPTER 79
a role. Almost all mortality is now related to associated anomalies of other organ systems,
primarily those of the heart, lungs, and brain.
22;
REFERENCES
Adzick NS, Harrison MR, deLorimier AA: Tapering duo- denoplasty for megaduodenum
associated with duodenal atresia. J Pediatr Surg 1986;21:311.
Akhtar J, Guiney EJ: Congenital duodenal obstruction. Br J Surg 1992;79:133.
. Alexander F, DiFiore J, Stallion A: Triangular tapered
duodenoplasty for the treatment of congenital duodenal obstruction. J Pediatr Surg
2002;37:862.
. Arnbjornsson E, Larsson M, Finkel Y, Karpe B: Trans-
anastomotic feeding tube after an operation for duodenal atresia. Eur J Pediatr Surg
2002;12:159.
. Andrassy RJ, Mahour GH: Gastrointestinal anomalies
associated with esophageal atresia or tracheoesophageal fistula. Arch Surg 1979;114:1125.
. Arey LB: Developmental Anatomy: A Textbook and
Laboratory Manual of Embryology, 7th ed. Philadelphia, WB Saunders, 1974.
. Bailey PV, Tracy TFJ, Connors RH, et al: Congenital duode-
nal obstruction: A 32-year review. J Pediatr Surg 1993;28:92.
. Bax NM, Ure BM, van der Zee DC, van Tuijl I: Laparoscopic
duodenoduodenostomy for duodenal atresia. Surg Endosc 2001;15:217.
. Bickler SW, Harrison MW, Blank E, Campbell JR:
Microperforation of a duodenal diaphragm as a cause of paradoxical gas in congenital
duodenal obstruction. J Pediatr Surg 1992;27:747.
Boyden EA, Cope JG, Bill AHJ: Anatomy and embryology of congenital intrinsic obstruction
of the duodenum. Am J Surg 1967;114:190.
Brown RA, Millar AJ, Linegar A, et al: Fenestrated duode- nal membranes: An analysis of
symptoms, signs, diagnosis, and treatment. J Pediatr Surg 1994;29:429,
Calder E: Two examples of children born with preternatural conformation of the guts. Med
Essays (Edinburgh) 1733;1:203. Celli J, van Bokhoven H, Brunner HG: Feingold syndrome:
Clinical review and genetic mapping. Am J Med Genet 2003;122A:294.
Chasen ST, Sharma G, Kalish RB, Chervenak FA: First- trimester screening for aneuploidy
with fetal nuchal translucency in a United States population. Ultrasound Obstet Gynecol
2003;22:149.
Cordes L: Congenital occlusion of the duodenum. Arch Pediatr 1901;18:401.
Dalla Vecchia LK, Grosfeld JL, West KW, et al: Intestinal atresia and stenosis: A 25-year
experience with 277 cases. Arch Surg 1998;133:490.
Danismend EN, Brown N: Morbidity and mortality in duodenal atresia. Z Kinderchir
1986;41:86.
de Lorimier AA: Bowel motility in infants and children born with duodenal atresia and
stenosis. J Pediatr Surg 1998;33:950.
Dewan LA, Guiney EJ: Duodenoplasty in the management of duodenal atresia. Pediatr Surg
Int 1990;5:253.
Ein SH, Shandling B: The late nonfunctioning duodenal atresia repair. J Pediatr Surg
1986;21:798.
Ein SH, Kim PC, Miller HA: The late nonfunctioning duodenal atresia repair—a second look.
J Pediatr Surg 2000;35:690.
Elliot GB, Kliman MR, Elliot KA: Pancreatic annulus: A sign or cause of duodenal
obstruction. Can J Surg 1968;11:357.
23
34,
1267
Duodenal Atresia and Stenosis—Annular Pancreas
Endo M, Ukiyama E, Yokoyama JMK: Subtotal duodenec- tomy with jejunal patch for
megaduodenum secondary to congenital duodenal malformation. J Pediatr Surg 1998;
33:1636.
Ernst NP: A case of congenital atresia of the duodenum treated successfully by operation.
BMJ 1916;1:1644. Escobar MA, Ladd AP, Grosfeld JL, et al: Duodenal atresia and stenosis:
Long-term follow-up over 30 years. J Pediatr Surg 2004;39:867.
Eustace S, Connolly B, Blake N: Congenital duodenal obstruction: An approach to diagnosis.
Eur J Pediatr Surg 1993;3:267.
Ferraris VA, McPhail JF: Adult duodenal web associated with peptic ulcer disease. Surg
Gynecol Obstet 1984;158:461. Fonkalsrud EW, DeLorimier AA, Hays DM: Congenital atresia
and stenosis of the duodenum: A review compiled from the members of the Surgical
Section of the American Academy of Pediatrics. Pediatrics 1969;43:79. Gahukamble DB,
Khamage AS, Shaheen AQ: Duodenal atresia: Its occurrence in siblings. J Pediatr Surg 1994;
29:1599.
Girvan DP, Stephens CA: Congenital intrinsic duodenal obstruction: A twenty-year review
of its surgical management and consequences. J Pediatr Surg 1974;9:833.
Gluer S, Petersen C, Ure BM: Simultaneous correction of duodenal atresia due to annular
pancreas and malrotation by laparoscopy. Eur J Pediatr Surg 2002;12:423.
Gray SW, Skandalakis JE: Embryology for Surgeons: The Embryological Basis for the
Treatment of Congenital Defects. Philadelphia, WB Saunders, 1986.
Grosfeld JL, Rescorla FJ: Duodenal atresia and stenosis: Reassessment of treatment and
outcome based on antenatal diagnosis, pathologic variance, and long-term follow-up. World
J Surg 1993;17:301.
Grosfeld JL, Ballantine TV, Shoemaker R: Operative man- agement of intestinal atresia and
stenosis based upon pathologic findings. J Pediatr Surg 1979;14:368.
Haeusler MC, Befghold A, Stoll C, et al: EUROSCAN Study Group: Prenatal ultrasonographic
detection of gastroin- testinal obstruction: Results from 18 European congenital anomaly
registries. Prenat Diagn 2002;22:616.
Hancock BJ, Wiseman NE: Congenital duodenal obstruc- tion: The impact of an antenatal
diagnosis. J Pediatr Surg 1989;24:1027.
Hendricks SK, Sybert VP: Association of annular pancreas and duodenal obstruction—
evidence for Mendelian inher- itance? Clin Genet 1991;39:383.
Hutton KA, Thomas DF: Tapering duodenoplasty. Pediatr Surg Int 1988;3:132.
Irving IM: Duodenal atresia and stenosis: Annular pan- creas. In Lister J, Irving IM (eds):
Neonatal Surgery, London, Butterworths, 1990, p 424.
Jona JZ, Belin RP: Duodenal anomalies and the ampulla of Vater. Surg Gynecol Obstet
1976;143:565.
Kaldor J: Atresia of the duodenum and duodenal diverticula. Ann Surg 1929;89:6.
Kamisawa T, Yuyang T, Egawa N, et al: A new embryologic hypothesis of annular pancreas.
Hepatogastroenterology 2001;48:277.
Kiernan PD, ReMine SG, Kiernan PC, et al: Annular pancreas: Mayo Clinic experience from
1957 to 1976 with review of the literature. Arch Surg 1980;115:46.
Kimble RM, Harding J, Kolbe A: Additional congenital anom- alies in babies with gut atresia
or stenosis: When to investigate and which investigation. Pediatr Surg Int 1997;12:565.
Kimura K, Tsugawa C, Ogawa K, et al: Diamond-shaped anastomosis for congenital
duodenal obstruction. Arch Surg 1977;112:1262.

You might also like