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13113 Dealing with Dumping Syndrome
sweet or sweetened foods) should be eliminated
from the diet to prevent late dumping symptoms.
Protein (e.g., meat, fish, chicken, eggs) and fat
intake should be increased to meet daily caloric
needs because of the restricted intake of carbohydrates. Many patients modify their diet according
to their personal experiences with food tolerance.
Most individuals with relatively mild symptoms will respond to dietary changes. For patients with severe vasomotor symptoms (postprandial hypotension), lying supine for 30 min
after meals may minimize the chance of syncope
by delaying gastric emptying and improving venous return. Supplementation of dietary fibers
(bran, methylcellulose) with meals has been
proven effective in the treatment of hypoglycemic episodes. Increasing the viscosity of food,
which slows down gastric emptying, is another
approach to improve dumping symptoms. Fifteen grams of guar gum or 5
meal
has been tested with good results, especially
in the pediatric population [25, 26]. However, the
palatability and tolerability of these supplements
is poor. Moreover, these substances are usually
not readily available as pharmaceutical products
at sufficiently high doses.
g of pectin with each
significantly blunts the postprandial rise of glucose and insulin by delaying carbohydrate digestion. Because of the reversible nature of the
inhibitor–enzyme interaction, the conversion of
complex carbohydrates (starch and sucrose) to
monosaccharides is delayed rather than completely blocked. This mechanism is responsible
for the effectiveness of acarbose in late dumping. The positive effects of acarbose have been
documented after a test meal in a few studies
(Table
13.2). In a double-blinded study of nine
patients
dose of 50 mg following a normal carbohydraterich meal has been shown to reduce the symptoms of postprandial hypoglycemia, especially in
combination with pectin [27]. A higher dose of
acarbose (100 mg) has not been found to have
any beneficial effect.
only the symptoms of late dumping, owing to the
mode of action of acarbose. In addition, acarbose
treatment often results in bloating, flatulence,
and diarrhea, as the unabsorbed carbohydrates
undergo bacterial fermentation in the small intestine; despite the decrease in these symptoms with
time, these adverse effects might hamper treatment compliance.
after gastric surgery, acarbose given at a
This treatment approach, however, affects
Pharmacologic Therapy
In approximately 3–5 % of patients, severe
dumping will continue despite dietary modifications. This results in marked weight loss, fear of
eating and outdoor activities, or even an inability
to maintain full-time employment. Drug therapy
plays an important role in patients who failed dietary changes.
Acarbose
Acarbose is an α-glucosidase inhibitor that interferes with carbohydrate absorption in the small
intestine. It is a generic drug sold in Europe and
Asia as Glucobay (Bayer AG), in North America as Precose (Bayer Pharmaceuticals), and
in Canada as Prandase (Bayer AG). Acarbose
Somatostatin Analogs
Somatostatin and its analog octreotide (Sandostatin®) [28] cause decreases in several GI
peptides (insulin, glucagon, VIP, GIP, neurotensin, etc.) that usually increase after meals.
In addition, these compounds directly decrease
gastric emptying and bowel motility, leading to
decreased nutritional absorption and blood flow
in the bowel [29]. As such, these analogs show
a broad range of activity against the full spectrum of symptoms of dumping syndrome. Both
fast-acting and delayed-release somatostatin analogs have been used in the treatment of dumping
syndrome. Fast-acting or long-acting repeatable
(LAR) formulations of octreotide are the agents
that have been most commonly studied [14, 28,
30–35].
132 K. H. Pak and S. H. Noh
Table13.2 Summary of studies that evaluated the effect of acarbose in dumping syndrome
Study No. of patients Treatment Result
McLoughlin et al. (1979) 10 Acarbose 100 mg; single admin-
Gerard et al. (1983) 24 Acarbose 100 mg; single admin-
al. (1985) 13 Acarbose 50 mg; single
Lyons et
Hasegawa et
GIP glucose-dependent insulinotropic polypeptide (also known as gastric inhibitory polypeptide), OGTT oral glucose
tolerance test, VIP vasoactive intestinal peptide
al. (1998) 6 Acarbose 50–100 mg; 3 times
istration before OGTT
istration before OGTT
administration before standard
breakfast
daily before meals for a month
Improved symptoms and glycemia during OGTT; reduced rise in plasma levels of GIP and insulin
Improved glycemia during OGTT;
reduced increase in plasma insulin
level; inhibition of glucose-induced
glucagon suppression
Significant attenuation of hyperglycemia; reduced rise in plasma levels of
GIP, enteroglucagon, and insulin; no
influence on plasma levels of VIP and
somatostatin; no significant effect on
symptoms
Attenuation of glucose fluctuations
improvement of dumping symptoms
(uncontrolled)
and
Studies of the Fast-Acting Somatostatin Analog Octreotide
The results of several short-term studies of
subcutaneously administered octreotide have
shown efficacy in improving symptoms, improving glycemia, and slowing gastric emptying
(Table 13.3) [30–33]. However, the need for 3–4
daily injections is potentially a major limitation
for the long-term application of fast-acting somatostatin analogs. Three studies have evaluated the
long-term use of subcutaneously administered
octreotide in the treatment of dumping syndrome.
Geer et al. found that long-term octreotide therapy (15 months on average) provided sustained
symptom control [32]. Out of ten patients, eight
received three daily injections of 100 μg octreotide, which resulted in good symptom control;
seven individuals were able to resume work.
Similarly, Vecht et al. evaluated the long-term
effect of three daily doses of 25–200 μg octreotide in 20 patients with a mean follow-up of
37 months [36]. All patients had an initial positive response; at 3 months, 80 % continued this
positive response. After 10 years, however, 11
of the 20 patients had discontinued therapy for
a variety of reasons, including a lack of effect
at 3 months ( n = 4), diarrhea ( n = 4), painful in-
jections ( n = 1), reversible alopecia ( n = 1), and
weight loss ( n = 1). Similar data were obtained
in a larger group of patients, in whom long-term
effects seemed less favorable than short-term
effects, although 41 % of the cohort continued
octreotide therapy after the follow-up period of
93 ± 15 months [34].
Studies of Long-Acting Octreotide LAR
Slow-release preparations of somatostatin analogs, which require only monthly intramuscular
injections, are an attractive alternative to multiple
daily injections of fast-acting formulations. Two
studies have investigated the efficacy of a slowrelease preparation of octreotide in dumping
syndrome. Penning et al. compared the efficacy
of monthly octreotide LAR (10 mg) to subcutaneous octreotide and found both formulations to
be effective at improving symptoms [35]. The
long-acting form seemed superior at increasing
body weight and improving quality of life. The
10 mg dose is only available in a limited number
of countries; the 20 mg dose is the usual standard
dose for LAR octreotide.
A multicenter study in Belgium confirmed
the efficacy of monthly LAR octreotide (20 mg)
in the treatment of dumping syndrome that was
refractory to dietary measures and acarbose
treatment [14]. The study compared the control
of symptoms and underlying pathophysiological mechanisms after 3 days of subcutaneous
treatment with octreotide (50 μg, 3 times daily)
with 3 months of treatment with octreotide LAR
13313 Dealing with Dumping Syndrome
Table13.3 Summary of studies that evaluated the effect of octreotide in dumping syndrome
Study No. of patients Treatment Result
Hopman et al. (1988) 12 Octreotide 50 mg vs. placebo
Primrose and Johnson[28] 10 Octreotide 50
Tuiassay et
Geer et
Richards et
Gray et
Hasler et
Arts et al. [14] 30 Octreotide 50 mg before OGTT Suppression of rise in pulse rate and
GIP glucose-dependent insulinotropic polypeptide (also known as gastric inhibitory polypeptide), OGTT oral glucose
tolerance test, VIP vasoactive intestinal peptide
al. (1989) 10 Octreotide 50 mg vs. placebo
al. [32] 10 Octreotide 100 mg vs. placebo
al. [33]
al. (1991) 9 Octreotide 100 mg vs. placebo
al. (1996) 8 Octerotide 50 mg vs. placebo
6 Octreotide 100
before OGTT
mg vs. 100 mg vs.
placebo before OGTT
before OGTT
before a dumping-provocative
meal
mg vs. placebo
before a dumping-provocative
meal
before a dumping-provocative
meal
before OGTT
Improved dumping symptoms and
suppression of postprandial rise in
pulse rate; reduced peak insulin and
increased nadir glycemia; slowing of
gastrointestinal transit
Reduced early dumping and abolished late dumping symptoms; sup
pression of early dumping-associated
changes in hematocrit and pulse rate;
inhibition of hypoglycemia
Suppression of rise in pulse rate
and hematocrit; suppression of rise
in plasma levels of VIP; inhibition of postprandial hypoglycemia;
inhibition of rise in plasma levels of
insulin and GIP
Prevention of development of dumping symptoms and diarrhea; prevention of late hypoglycemia and of
the rise in plasma levels of glucose,
glucagon, pancreatic polypeptide,
neurotensin and insulin; delayed gastric emptying and intestinal transit
Prevention of dumping symptoms;
induction of migrating motor complex phase III in the small intestine;
decreased postprandial intestinal
motor activity
Suppression of rise in pulse rate;
inhibition of insulin release; prevention of hypoglycemia; inhibition of
dumping symptoms
Suppression of rise in pulse rate;
inhibition of dumping symptoms
and diarrhea; no influence on change
in hematocrit; inhibition of insulin
release; prevention of hypoglycemia;
no influence on gastric emptying rate
hematocrit; inhibition of postprandial
hypoglycemia; inhibition of rise in
plasma levels of insulin; improvement of early and late dumping
symptoms
-
at 20 mg. Both the fast-acting and long-acting
formulations had a favorable effect on dumping
symptoms, glycemia, and pulse rate during provocative testing for dumping. The fast-acting
form showed greater efficacy than the long-acting form in improving hypoglycemia. However,
treatment with the long-acting formulation was
associated with a significant improvement in
patients’ quality of life and was markedly preferred by recipients over the fast-acting preparation [14].
134 K. H. Pak and S. H. Noh
Adverse Effects of Somatostatin Analogs
The main adverse events related to the use of somatostatin analogs are pain at the site of injection, gallstone formation, and the occurrence of
steatorrhea. The latter symptom is usually mild,
and the long-term use of somatostatin analogs is
usually associated with weight gain of approximately 1 % in spite of the occurrence of steatorrhea. Gallstone formation is not an uncommon
complication of the long-term use of somatostatin analogs and should be taken into account
when considering treatment options for dumping syndrome [37, 38]. Another disadvantage of
somatostatin analogs is their considerable cost.
For this and the aforementioned reasons, treatment with somatostatin analogs is not the firstline treatment option for patients with dumping
syndrome. However, dumping syndrome is associated with significant impairment of quality of
life, and the improvement in this parameter with
somatostatin analogs is impressive. The development of an oral or nasal formulation should further improve the application of octreotide in the
treatment of dumping syndrome [14, 32].
Surgical Treatment
Conservative management is always preferred
because most patients will exhibit improvement
in dumping over time, and surgery may not be
curative. Postgastrectomy syndromes often abate
with time. Therefore, medical, dietary, and behavioral therapy should be given at least a 1-year
trial. If these nonoperative measures fail, corrective surgery may be considered.
Conversion of Billroth II to Billroth I Anastomosis
This procedure restores the physiological delivery of the meal to the duodenum without creating
the risk of gastric outlet obstruction. Woodward
et al. reported an improvement in dumping syndrome in 75 % of patients [39]. The procedure
has a low rate of complications and is relatively
simple.
Roux-en-Y Conversion
A conversion to a Roux-en-Y gastrojejunostomy
is preferred as a remedial operation [40]. RYGJ
is useful in patients with dumping because it
slows down gastric emptying and the transit of
chyme through the Roux limb. The mechanisms
responsible for the effectiveness of this surgery
in dumping are not well known. However, the interruption of the migration motor complex and
diminished jejunal contractions may play a major
role. Favorable outcomes have been reported
after this operation in 85–90
Billroth I and II gastrectomy
[18] reported
with this operation. This procedure is easier to
perform and has fewer long-term complications
(e.g., Roux stasis syndrome) [41].
Overall, surgery has a limited role in the treatment of dumping. Selection of the appropriate
surgical procedure is very important. In terms of
remedial operations for patients following pyloroplasty, pyloric reconstruction should be the
initial corrective operation. Roux-en-Y reconstruction appears to be the most effective option
for patients with Billroth I and Billroth II gastrectomies. For those patients who already have
a Roux-en-Y reconstruction, an antiperistaltic
jejunal segment can be interposed.
excellent results in 19 of 22 patients
% of patients with
[16, 17]. Vogel et
al.
Continuous Enteral Feeding
A final approach to the treatment of patients with
refractory dumping syndrome is the creation of
a feeding jejunostomy, through which a continuous background flow of nutrients can be provided. This is a rather invasive intervention, with
a major effect on daily life, but it appears to be
effective in avoiding symptoms that are triggered
by meal ingestion [42].
Conclusion
Dumping syndrome is a common complication
after gastric surgery. Clinically significant dumping can result in serious distress and considerable
morbidity in patients. The diagnosis of dumping
syndrome is based on clinical presentation, and if
needed, it can be confirmed by a provocation test
13513 Dealing with Dumping Syndrome
with oral glucose. With regard to gastric surgery,
Billroth I or R-Y gastrojejunostomy after distal
gastrectomy is better than Billroth II for the prevention of dumping syndrome. The majority of
patients respond to dietary modifications. Therapy with octreotide is an effective alternative prior
to considering surgical correction. Close attention must be given to the patient’s nutritional status. If medical therapy fails to provide symptom
relief, surgical revision should be offered, with
the understanding that even this intervention may
not be successful.
Key Points
1. Dumping syndrome is a common complication of esophageal and gastric (including bariatric) surgery.
2. Symptoms include early (gastrointestinal and
vasomotor) and late (hypoglycemia) symptoms.
3. Diagnosis is based on a suggestive symptom
pattern in patients with the appropriate surgical history; a modified oral glucose tolerance
test might help to establish the diagnosis.
4. To prevent dumping syndrome, Billoth I or
R-Y gastrojejunostomy after distal gastrectomy is preferred over Billroth II.
5. Initial therapy should focus on dietary measures.
6. In patients who have not responded to initial
therapy (slow-release), somatostatin analogs
are the treatment of choice.
7. In patients with treatment-refractory dumping
syndrome, surgical reintervention or continuous enteral feeding can be considered, but the
outcomes of such approaches are variable.
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-
Aerent Loop Syndrome
Georey W. Krampitz, Graham G. Walmsley
and Jerey A. Norton
14
Introduction
Afferent loop syndrome (ALS) is a constellation
of signs and symptoms caused by mechanical obstruction of the afferent loop following surgical
construction of a double-barrel gastrojejunostomy (Fig. 14.1a). The afferent loop consists of the
segment of duodenum and/or proximal jejunum
upstream of a double-barrel gastrojejunostomy
anastomosis. Accumulation of enteric secretions
in the obstructed afferent loop causes increased
intraluminal pressure leading to symptoms of abdominal pain and distension. ALS can be classified into acute and chronic forms. Acute ALS is
due to complete obstruction of the afferent loop,
usually occurring within 1 week after surgery.
Chronic ALS is due to partial obstruction of the
afferent loop, usually occurring several months
or years after surgery. McNealy first described
acute ALS as a cause of early postoperative duodenal stump leak in 1942 [1]. In 1948, Lake first
described chronic ALS as obstruction of free passage of duodenal contents across the anastomosis leading to “afferent loop stasis” [2]. In 1950,
J. A. Norton () · G. W. Krampitz · G. G. Walmsley
Department of Surgery, Stanford University School of
Medicine, 300 Pasteur Dr., H3591, Stanford, CA 943055655, USA
e-mail: janorton@stanford.edu
G. W. Krampitz
e-mail: krampitz@stanford.edu
G. G. Walmsley
e-mail: grahamw@stanford.edu
Roux coined the terms “afferent loop syndrome”
when describing the condition in partially
gastrectomized patients [3]. Because the symptoms associated with ALS are nonspecific, these
conditions can be difficult to diagnose. However,
if unrecognized, ALS can lead to significant morbidity and mortality and consequently requires a
high index of suspicion and prompt treatment.
Epidemiology
In 1955, Jordan initially reported an incidence
of 0.3 % of afferent loop syndrome complicating partial gastrectomies [4]. Historically, ALS
was associated with gastrectomy with Billroth II
reconstruction, with an incidence of up to 20 %
[5]. At that time, many of these operations were
performed for peptic ulcer disease. However,
given the precipitous decline in elective operations for complications of ulcer disease, [6],, the
contemporary incidence of ALS is unclear. More
recently, Aoki retrospectively reviewed the cases
of 1908 patients who underwent open distal gastrectomy between 1999 and 2008. He found that
0.2 % of these patients developed ALS. Pannala
reported that the incidence of ALS in a cohort of
186 pancreatic cancer patients after pancreaticoduodenectomy was as high as 13 % [7]. Kim retrospectively reviewed a surgical database of 396
patients who underwent laparoscopic distal gastrectomy with Billroth II reconstruction between
2004 and 2011 and found an incidence of ALS of
1.01 % [8]. Therefore, the estimated current inci-
T. M. Pawlik et al. (eds.), Gastrointestinal Surgery, DOI 10.1007/978-1-4939-2223-9_14,
© Springer Science+Business Media New York 2015
137
138 G. W. Krampitz et al.
Fig. 14.1 Afferent loop obstruction in a 62-year-old
man after Roux-en-Y gastroenterotomy. a Axial plane of
MDCT shows a dilated fluid-filled afferent loop ( arrow)
located at the mid-abdomen and crossing between the
aorta and superior mesenteric artery. b Coronal plane of
MDCT reveals the configuration of the afferent loop to
be of a “C” character. c Keyboard sign ( arrows) is also
clearly demonstrated. Focal bowel thickening at the anastomotic region is present, suggesting local recurrence. Endoscopic biopsy confirmed the MDCT diagnosis of local
recurrence. (With permission from [28] © Copyright:
Yonsei University College of Medicine 2011; Creative
Commons Public License: http://creativecommons.org/
licenses/by-nc/3.0/legalcode. Used without modification)
to bowel necrosis and perforation. This occurs
because typically the surgeon is not considering
ALS in the differential diagnosis. The mortality
rate reported before the development of CT or ultrasound was as high as 30–60 % [9].
Etiology
The likelihood of developing ALS is influenced
by both surgical technique and postoperative
complications. The syndrome generally occurs
when the afferent limb is longer than 30–40 cm
and has been anastomosed to the gastric remnant
in an antecolic fashion [10]. A variety of factors can contribute to the development of ALS,
including kinking and angulation of the afferent
limb, internal herniation behind the efferent limb,
stenosis of the gastrojejunal anastomosis, redundant twisting of the afferent limb with resultant
volvulus, or adhesions involving the afferent
limb. ALS can also result from a failure to close
mesocolic defects following construction of retrocolic gastrojejunostomy.
Several conditions following gastrojejunostomy can lead to ALS. Presentations of ALS
with enterolith tend to be rare and late onset [11].
Several case reports have documented cases of
chronic ALS related to large duodenal stones as
late as 24 years postsurgery [12, 13]. Hui et al.
reported a case of a 10-year presentation of ALS
postgastric surgery with a large duodenal phytobezoar [14]. Other postoperative causes of ALS
following gastrojejunostomy include scarring
due to anastomotic ulcers [15], internal hernia
[16], and intestinal volvulus [17]. Cancer recurrence near the site of anastomosis causing ALS,
often termed malignant ALS, has been reported
frequently in patients with pancreatic cancer with
widespread carcinomatosis resulting in twisting
or obstruction of the afferent limb [18].
Pathophysiology
dence is between 0.2 and 13 %, with a guestimate
incidence of 1–2 %. Mortality from ALS is
typically the result of a delay in diagnosis leading
Complete or partial obstruction of the afferent
limb as a technical issue at the time of surgery
causes acute ALS and potentially chronic ALS.
13914 Afferent Loop Syndrome
Complete or partial obstruction along the jejunal
portion of the efferent loop results in entry of
gastric chyme into the afferent loop, triggering
the release of enteric hormones. Accumulation of
bile, water, pancreatic secretions, and bicarbonate in the afferent loop causes abdominal distension and increased intraluminal pressure. Postoperative ascending cholangitis [19], obstructive
jaundice [20], and pancreatitis [21] may ensue.
Bile acid malabsorption may occur due to bacterial overgrowth and result in accompanying irondeficiency anemia, megaloblastic anemia due to
B12 deficiency, bleeding due to vitamin K deficiency, and Wernicke syndrome due to deficits in
vitamin B1 [22]. Intestinal stasis resulting in bacterial overgrowth and steatorrhea, vitamin B12,
folic acid, and iron deficiency is often termed
“blind loop syndrome.”
Clinical History
Patients with acute ALS frequently present with
sudden onset right upper quadrant abdominal
pain, nausea, and nonbilious vomiting. Acute
ALS is considered a surgical emergency and typically occurs in the early postoperative period but
has also been reported to occur 30 years after surgery. The risk of intestinal perforation/infarction
and disruption of the duodenal stump necessitates prompt decompression of the afferent loop.
Patients with chronic ALS typically experience postprandial epigastric pain and abdominal
distension lasting from several minutes to an
hour. Bilious projectile vomiting is a common
manifestation of chronic ALS and provides rapid
symptom relief. Intestinal stasis during chronic
ALS can be complicated by diarrhea and steatorrhea. Subsequent bacteria-mediated deconjugation of bile salts can result in vitamin B12 deficiency and/or iron-deficiency anemia. Patients
often stop eating to avoid postprandial pain and
may experience severe weight loss.
Physical Findings
The most common physical finding in ALS is
epigastric/right upper quadrant abdominal tenderness. Approximately one-third of patients
with acute ALS have a palpable right upper quadrant abdominal mass. Patients may present with
obstructive jaundice or abdominal pain radiating
to the back or flank indicative of pancreatitis.
If bowel perforation has occurred, patients may
present with a rigid abdomen and guarding indicative of peritonitis.
Differential Diagnosis
Because the physical findings associated with
ALS are nonspecific, there are a number of other
etiologies that must be considered. Among the
differential diagnosis for ALS are abdominal abscess, hernia, acute mesenteric ischemia, anemia,
bacterial overgrowth syndrome, bile duct strictures, bile reflux gastritis, biliary colic, bowel
obstruction, carcinoma of the ampulla of Vater,
choledochal cysts, choledocholithiasis, gastric
outlet obstruction, gastric sarcoma, gastric ulcer,
volvulus, gastritis, intestinal perforation, mesenteric thrombosis, mesenteric cyst, omental torsion, pancreatic pseudocyst, and tumors (gastric,
bile duct, small intestine, mesenteric). Given the
broad differential diagnosis, a detailed surgical
history and high clinical suspicion are imperative
to making an accurate diagnosis.
Diagnosis
Laboratory studies may aid in the diagnosis of
ALS; however, a confirmatory diagnosis necessitates imaging studies. Increased intraluminal
pressure accompanying ALS may be transmitted
to the biliary tract and cause ascending cholangitis, obstructive jaundice, or pancreatitis [23,
24]. A check for elevated levels of alkaline phos-
phatase, alanine/aspartate aminotransferases,
amylase, lipase, and serum bilirubin may aid the
diagnostician in this regard. Given the possible
presence of anemias related to ALS (vitamin B12
140 G. W. Krampitz et al.
deficiency, iron deficiency), a check for hemoglobin, hematocrit, mean corpuscular volume,
cell size, iron content, and WBC count may also
aid in the diagnosis of chronic ALS. In suspected
ALS patients, a serum electrolyte panel should
also be obtained to check for possible hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis due to vomiting and diarrhea that
may accompany ALS. Finally, a carbon 14 xylose breath test may detect bacterial overgrowth
due to intestinal stasis related to ALS.
Noninvasive Imaging Studies
Abdominal CT is considered the radiographic
study of choice in the diagnosis of ALS [25]. CT
scanning can directly visualize the obstructed
intestinal segment. Other structures such as the
pancreas and biliary tree that may be impacted
by the obstruction can also be examined. ALS
typically presents as a fluid-filled tubular structure crossing the abdominal midline between the
aorta and super mesenteric artery, and the radiographic appearance was first described in 1980
by Kuwabara et al. [26]. CT scanning has also
proven useful in predicting the pathology underlying ALS. Kim et al. found that CT scanning
helped correctly predict internal herniation, adhesions, and recurrent gastric cancer as the underlying etiology for ALS in all 18 patients examined
[27]. Juan assessed the multidetector computed
tomography (MDCT) findings of ALS in a retrospective study of 1100 patients who underwent
gastroenterostomy reconstruction between 2004
and 2008. Of the 2 % of patients diagnosed with
ALS, 100 % had a fluid-filled C-shaped afferent
loop and 98 % had valvulae conniventes projecting into the lumen (keyboard sign) on MDCT
(Fig. 14.1) [28].
In patients with ALS, abdominal ultrasound
may reveal a fluid-filled mass in the right upper
quadrant or a peripancreatic cystic mass. Derchi
et al. identified the distended afferent limb as a
fluid-filled structure in four patients with ALS
caused by tumor recurrence at or near a Billroth
II gastrojejunostomy [29]. Lee et al. reported
similar findings in a study of seven ALS patients,
observing the obstructed afferent limb as a dilated, fluid-filled structure crossing the midline in
the upper abdomen [30].
In patients in whom ultrasound and endoscopy are nondiagnostic, hepatobiliary scintigraphy
may prove useful in diagnosing chronic ALS.
Sivelli et al. used technetium-99 m hepatoaminodiacetic acid scanning in 50 patients and found
that hepatobiliary scanning is useful in diagnosing ALS [31]. Despite other studies showing success using mebrofenin and hepatoaminodiacetic acid scanning [17, 32], scintigraphic studies
should be reserved for cases where abdominal
CT and ultrasound are nondiagnostic.
Invasive studies such as esophagogastroduodenoscopy allow for direct visualization of the
gastrojejunostomy and detection of possible
modes of obstruction (i.e., volvulus, herniation,
ulceration, etc.). In addition to identifying possible masses in the region of the gastrojejunostomy, esophagogastroduodenoscopy can be helpful
in distinguishing between alkaline reflux gastritis
and ALS [10].
Treatment
Medical Treatment
Acute ALS requires immediate diagnosis and
corrective surgery. Indeed, the major pitfall associated with ALS is a delay in diagnosis due to
risk of intestinal perforation and sepsis [33]. Patients with chronic ALS may develop malnutrition or anemia [22, 34], and may derive benefit
from nutritional therapy or transfusion prior to
surgery.
Endoscopic/Interventional Radiology
Although surgical conversions have been the
treatment of choice, percutaneous tube drainage
or stent placement has been performed as a palliative treatment for patients who cannot tolerate
a surgical procedure. Metallic stents have been
used for the relief of afferent loop syndrome due
to number of etiologies [35–37]. In a 77-year-