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may be necessary for obstruction, or the diagnosis of lymphoma
may be made postoperatively after surgical intervention for small
bowel obstruction (SBO) has already taken place. In patients without
signs and symptoms of SBO, CT-guided or endoscopic biopsy is
appropriate to guide therapy. Indeed, the main role of biopsy in small
bowel tumors is to distinguish lymphoma, as most other small bowel
masses require resection as the primary management.
Metastatic Disease
Secondary involvement of the small bowel from other metastatic
lesions presents as multifocal advanced cancer and not as an isolated
small bowel lesion. Lung, melanoma, breast, colon, and cervical cancers can all spread to the small bowel. Sarcomas and adenocarcinomas can also impact the small bowel, either through direct erosion or
carcinomatosis of overlying peritoneum. As an innocent bystander,
the small bowel may need to be resected or bypassed depending on
the type and stage of primary tumor.
SUMMARY
Small bowel tumors are rare and present with a constellation of
common symptoms. Late diagnosis makes the prognosis of small
bowel malignancy particularly poor, and a thorough workup to
rule out small bowel tumors should be undertaken in anyone with
vague abdominal pain and paraneoplastic symptoms with no other
apparent source. Aside from small bowel lymphoma, most other
suspicious small bowel masses do not require biopsy and should be
FIG. 7 Small bowel lymphoma.
resected. Nuanced management of these malignant lesions has room
for investigation, and surgeons should feel compelled to lead efforts
to discover optimal treatment paradigms and create guidelines.
intestinal lesion is a rare presentation for lymphoma. Patients with
Celiac disease have a 20-fold higher risk of GI lymphoma, and
patients with chronic immunosuppression including transplant
recipients and those with HIV are also at an increased risk. On CT
with IV contrast, the mass often appears well circumscribed and
homogeneous (Fig. 7).
A tissue diagnosis is required for lymphoma, and as there are a
variety of non-Hodgkin subtypes, it is imperative that enough tissue
is harvested to perform the full battery of cytopathology and flow
cytometry. The subtype dictates the tumor behavior, treatment, and
prognosis. Most small bowel lymphomas do not require resection and
rather are best treated with multidrug chemotherapy. The 5-year survival is 50%, with poorer prognosis in males and the elderly. Surgery
Small Bowel
Diverticulosis
Jonathan B. Greer, MD
INTRODUCTION
Although small bowel diverticulosis is a rare clinical entity, all general
surgeons should be comfortable with its diagnosis and management.
The true prevalence is unknown, but a busy practitioner will frequently encounter these in clinical practice. Less than 4% of all small
bowel diverticula will become overtly symptomatic. The duodenum
S u g g e S t e d R e a d i n g S
Cross AJ, Leitzmann MF, Subar AF, et al. A prospective study of meat
and fat intake in relation to small intestinal cancer. Cancer Research.
2008;68:9274.
Leoncini E, Carioloi G, La Vecchia C, etal. Risk factors for neuroendocrine
neoplasms: a systematic review and meta-analysis. Annals of Oncology.
2016;27:68.
Miettinen M & Lasota J. Gastrointestinal Stromal Tumors: Review on
Morphology, Molecular Pathology, Prognosis and Differential Diagnosis.
Archives of Pathology and Laboratory Medicine. 2006:1466–1478.
Min KW, Leabu M. Interstitial cells of Cajal (ICC) and gastrointestinal stro-
mal tumor (GIST): facts, speculations, and myths. Journal of Cellular and
Molecular Medicine. 2006;10(4):995–1013.
is the most common site, while Meckel’s diverticula are the most wellknown. Small bowel diverticula can be congenital or acquired. These
can be classified as either true or false, based on whether all three
walls of the bowel are involved. Meckel’s diverticula are the most wellknown true diverticula of the small bowel. They are further classified
by location (duodenal or jejunoileal), but they are best delineated
by those that are asymptomatic and therefore incidentally detected
versus those that present with clinical symptoms (usually bleeding
or diverticulitis) and rarely as a cause of obstruction or perforation.
Many manuscripts have been published on this topic, mostly single-center studies or case reports. There is a paucity of high-level
evidence, however. Nonetheless, improvements in both axial imaging
and advanced endoscopic techniques will likely lead to the increased
detection of small bowel diverticulosis over time. This chapter will
review the diagnosis and management of this clinical entity.
150 SMALL BOWEL DIVERTICULOSIS
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DETECTION AND MANAGEMENT OF
ASYMPTOMATIC (INCIDENTALLY
DISCOVERED) SMALL BOWEL
DIVERTICULOSIS
The increasing frequency of high-quality cross-sectional imaging
and endoscopic procedures has led to an increase in the detection of
asymptomatic small bowel diverticulosis. However, this has not led
to an increase in symptomatic cases. There are three principal groups
of asymptomatic small bowel diverticula: duodenal, jejunoileal, and
Meckel’s diverticula, a subset of jejunoileal diverticula that are always
congenital and true diverticula.
Duodenal Diverticula
The most common diverticula of the small bowel are duodenal
diverticula, comprising 45% to 79% of cases. In terms of prevalence,
a true number is difficult to ascertain, but these have been reported
in 2% to 5% of upper gastrointestinal contrast studies, 7% of endoscopic retrograde cholangiopancreatography, and as high as 20%
in one autopsy series. The only known risk factor is age. Duodenal
diverticula are most commonly located in the second portion of the
duodenum (60% to 95% of cases). They are much more commonly
asymptomatic. These can be congenital or acquired, and extraluminal or intraluminal. The vast majority are acquired and extraluminal.
The mechanism is thought to relate to weakness of the bowel wall
where perforating vessels are found. There are rare congenital duodenal diverticula that are intraluminal, called windsock diverticula,
and are lined with duodenal mucosa on the entirety of the diverticulum, both inside and outside, from a failure of canalization of the
embryonal foregut.
Diagnosis is made by the discovery of an outpouching of the
duodenum on cross-sectional imaging, fluoroscopic contrast studies,
endoscopy, or at the time of an abdominal operation. Though duodenal diverticula can be quite large, asymptomatic diverticula are, by
definition, asymptomatic; therefore, no treatment is required. Particularly in cases that would require a pancreaticoduodenectomy, surgical resection is associated with significant morbidity and therefore
is not recommended for an incidentally discovered diverticulum.
Jejunoileal Diverticula
Jejunoileal diverticula are less common than duodenal diverticula,
comprising less than 20% of small bowel diverticulosis in most series,
although they are more likely to cause complications than their duodenal counterparts. The actual prevalence is unknown, but autopsy
series have reported a prevalence as high as 7%. The vast majority are
asymptomatic. These can be single or multiple, with 80% in the jejunum, 15% in the ileum, and 5% found in both. False diverticula are
the most common. These are likely caused by the gradual weakening
of the wall of the intestine from increased intraluminal pressure that
can be generated by dysfunction of the migrating motor complexes.
As such, age is the most widely reported risk factor. Other risk factors
include intestinal dysmotility disorders. The most common location
is the proximal jejunum, and these are frequently multiple.
Jejunoileal diverticula can be discovered on laparotomy, although
they are commonly also diagnosed on radiographic or endoscopic
studies. Enteroclysis is the best radiographic study to evaluate jejunoileal diverticula, though CT and MR enterography are increasingly
used as techniques improve. Capsule endoscopy may be useful as
well. There is no role for the surgical management of incidentally
discovered jejunoileal diverticula.
Meckel’s Diverticulum
Meckel’s diverticula are the most common congenital diverticula
of the small bowel and account for 25% of small bowel diverticula
(Fig. 1). A prevalence estimate in an autopsy study was 1.23%.
FIG. 1 Common presentation of a Meckel’s diverticulum projecting
from the antimesenteric border of the ileum. (From McKenzie S, Evers BM.
Small intestine. In: Townsend CM Jr, ed. Sabiston Textbook of Surgery. 19th ed.
Philadelphia: Elsevier; 2012.)
They are, by definition, true diverticula of the ileum and represent
a remnant vitelline (omphalomesenteric) duct that connects the
embryonic midgut to the yolk sac. This duct is normally obliterated
during embryologic development. As a true diverticulum, it involves
all three layers of the bowel wall and is always antimesenteric. The
classic “rule of two” for Meckel’s diverticula is thus: They are located
approximately 2 feet from the ileocecal valve, contain two types of
heterotopic tissue (gastric or pancreatic), occur twice as commonly
in males, in 2% of the population, are symptomatic in about 2% of
cases, tend to be diagnosed within the first 2 years of life, and can
extend over 2 inches in length. Additionally, there are two types of
symptoms that can arise: bleeding and obstruction.
Given their small size, most asymptomatic Meckel’s diverticula
are discovered during surgery for another indication. They are less
frequently found on axial imaging. Meckel’s diverticula have a low
lifetime risk of complications related to the diverticula itself, and
mortality is extremely rare. Therefore, in most cases, there is no
compelling indication for surgical resection of an incidentally discovered Meckel’s diverticulum in an adult. Some authors advocate for
prophylactic resection in children, and in adults in cases of palpable
ectopic tissue, prior history of diverticulitis, hemorrhage, intussusception, or the presence of a mesodiverticular band. This is in contradistinction to the management of clinically significant Meckel’s
diverticula, which will be discussed later in this chapter.
DETECTION AND MANAGEMENT
OF SYMPTOMATIC SMALL BOWEL
DIVERTICULOSIS
The minority of small bowel diverticula present with clinical
manifestations, which can be infection (diverticulitis), bleeding,
or obstruction. Unlike the incidentally discovered and therefore
asymptomatic versions, symptomatic small bowel diverticula require
treatment.
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Duodenal Diverticula
Only about 5% of patients with duodenal diverticula present with
complications. The most commonly reported symptom is postprandial epigastric abdominal pain, which can be associated with nausea
and vomiting. Obstruction from a duodenal diverticula is quite rare
but can occur, particularly in cases in which the diverticula is large.
This can result in extraluminal compression of the duodenum. There
can also be extrinsic compression of the biliary tree or pancreatic
duct, thus resulting in a rare cause of obstructive jaundice or recurrent pancreatitis. More commonly, infectious complications may
develop, such as diverticulitis +/– abscess, perforation, and rarely,
fistula. Bleeding may also occur secondary to diverticulitis as inflammatory erosion into a neighboring vessel may result in fairly significant bleeding, with hematemesis and melena as the presenting signs.
After initial nasogastric tube decompression for duodenal
obstruction, diagnosis of a duodenal diverticula as the underlying
cause is usually one of exclusion, as a malignancy would be far more
common. This diagnosis can be made by axial imaging, usually
CT, although an upper gastrointestinal contrast study may also be
helpful. These can be challenging in an obstructed patient. In conjunction with these radiographic studies, endoscopy is necessary to
rule out mucosal-based lesions as the etiology. In cases of biliary
tree or pancreatic duct obstruction from duodenal diverticula, axial
imaging (CT or MRI) in concert with endoscopy, including ERCP,
are essential to make the diagnosis. Duodenal diverticulitis will usually be diagnosed on CT with characteristic findings similar to the
vastly more common colonic diverticulitis. CT angiography may be
necessary to identify a bleeding vessel related to a duodenal diverticula, although endoscopy may also be helpful. The patient’s clinical
condition should dictate whether purely diagnostic studies (e.g., CT
angiography or endoscopy) can be safely done, rather than diagnostic and therapeutic modalities, such as mesenteric angiography in
interventional radiology.
Management of duodenal diverticulosis in the asymptomatic
patient is straightforward (nothing to do) but can be more nuanced
in symptomatic patients and varies greatly with the clinical scenario.
The rare case of duodenal obstruction secondary to a duodenal
diverticula may require surgical intervention. This may include
resection of the diverticula alone with transverse closure of the
duodenum, use of a serosal small bowel (Thal) patch, a Roux-en-Y
duodenojejunostomy, or potentially a segmental duodenal resection.
Assessment of the anatomic relationship between the ampulla of
Vater and the line of transection is crucial for segmental resection
of the duodenum. Involvement of the medial side of the duodenum
that results in obstruction will require a pancreaticoduodenectomy.
The more common case involving biliary or pancreatic obstruction
should be temporized first via endoscopic means, usually with stenting. Surgical resection, which would be a pancreaticoduodenectomy,
should be reserved for patients who fail endoscopic management. As
with all complex hepatobiliary procedures, surgeon familiarity and
comfort with these techniques along with well-delineated anatomic
relationships between the duodenal diverticula and important neighboring structures is critical. Most cases of duodenal diverticulitis,
even with contained perforation, can be managed conservatively
with nil per os, placement of a nasogastric tube, antibiotics, and
occasionally percutaneous drainage. Surgical management in the
acute setting is almost never indicated and can be quite challenging.
Bleeding duodenal diverticula are managed similar to other causes
of upper gastrointestinal bleeding, either via endoscopy or interventional radiology. Surgical management is rarely indicated.
Jejunoileal Diverticula
Symptomatic false jejunoileal diverticula are rare, but about 10%
of all jejunoileal diverticula will become symptomatic. Patients can
present with nonspecific symptoms such as abdominal pain, early
satiety, bloating, and malabsorption (diarrhea and/or steatorrhea)
secondary to small intestinal bacterial overgrowth (SIBO). The complications that can arise and therefore lead to detection are diverticulitis, bleeding, obstruction, or perforation. The clinical presentations
associated with each of these complications are similar to their large
bowel counterparts, although the pain is typically epigastric or periumbilical in location. Cross-sectional imaging is the most common
means of detection as these patients will usually present with abdominal pain or melena.
SIBO is treated with antibiotics. The treatment of jejunoileal
diverticulitis is identical to that of colonic diverticulitis: bowel rest,
intravenous fluids, and antibiotics. Surgical intervention is not always
needed, particularly in isolated cases. Recurrent or complicated episodes may mandate segmental resection, although rare. Management
of perforated jejunoileal diverticula depends greatly on the condition
of the patient. Conservative management may be appropriate in cases
in which the perforation has walled off and the patient is minimally
symptomatic. Conversely, critically ill patients warrant urgent exploration and segmental resection. Enterocutaneous fistulae secondary
to jejunoileal diverticulitis have been reported. A bleeding jejunoileal
diverticulum can be found on push or double-balloon enteroscopy
or on capsule endoscopy, and it should be considered in cases of gastrointestinal bleeding in which both esophagogastroduodenoscopy
and colonoscopy are negative. Endoscopic management of bleeding
can be difficult, and interventional radiology angioembolization is
not typically attempted. After a trial of conservative management,
surgical intervention is warranted. Small bowel obstructions secondary to jejunoileal diverticula are managed like adhesive small bowel
obstructions. Resection of the diverticula would be warranted in
cases of failure of conservative management. An uncommon clinical
scenario is bowel obstruction secondary to an impacted fecalith.
These can be treated surgical by enterotomy and stone extraction.
Meckel’s Diverticula
The risk of a complication that leads to discovery of a Meckel’s diverticulum is estimated to be in the 2% to 6% range. The most common
mechanism of a symptomatic Meckel’s diverticulum is thought to
relate to acid production by heterotopic gastric mucosa within the
diverticulum leading to ulceration. The symptoms/complications
that can arise are bleeding, obstruction, or abdominal pain. These
usually occur in the pediatric population. The relative proportion
of each of these findings is not fixed, but one single-center series of
known Meckel’s diverticula in pediatric patients had 19% discovered
incidentally, whereas the remaining patients presented with the
following: 35% gastrointestinal bleeding, 20% diverticulitis or perforation, 14% obstruction, and 12% intussusception.
Gastrointestinal bleeding that is caused by a Meckel’s diverticulum may be acute or chronic. It is frequently associated with heterotopic gastric mucosa, much more so than an asymptomatic Meckel’s
diverticulum. The suspicion of a bleeding Meckel’s diverticulum
should be higher in young patients with no evidence of an inflammatory explanation for the bleeding, such as infectious illnesses or
inflammatory bowel disease, or in adults <30 years of age in whom
an exhaustive workup for gastrointestinal bleeding is otherwise negative. Algorithms for gastrointestinal bleeding should be followed in
the appropriate clinical setting. A Meckel’s scan, which is a scintigraphic study, or mesenteric angiography may localize the Meckel’s
diverticulum as the source of the bleed, as can advanced endoscopic
techniques such as double-balloon or capsule endoscopy (Fig. 2). CT
angiography has been shown to play an increasing role as a sensitive
test, but in a young, hemodynamically stable patient, the Meckel’s
scan is the test of choice as it will detect heterotopic gastric mucosa
in 85% to 97% of cases. Rarely, if all other studies are negative, in the
setting of ongoing bleeding leading to hemodynamic compromise,
surgical exploration may be warranted to exclude a bleeding Meckel’s
diverticulum.
There are multiple mechanisms by which a Meckel’s diverticulum
can lead to a small bowel obstruction, including hernia formation. In
152 DIAGNOSIS AND MANAGEMENT OF MOTILITY DISORDERS OF THE STOMACH AND SMALL BOWEL IN THE CURRENT ERA
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Diverticulitis or perforation secondary to a Meckel’s diverticulum
will lead to abdominal pain and tenderness on physical examination.
Although the location of tenderness secondary to Meckel’s diverticulitis may be variable, perforation will lead to lower abdominal
Stomach
tenderness.
The treatment of a clinically significant Meckel’s diverticulum
is first to address the clinical scenario in a standard fashion. For
example, in the case of a bowel obstruction secondary to a Meckel’s
diverticulum, nasogastric tube decompression and volume resuscitation are the first steps. Following this, surgical resection should be
undertaken. Surgical resection can be either via a diverticulectomy
or segmental bowel resection and reconstruction. A segmental
resection is recommended in cases in which the base of the diverticulum is broad or there is a palpable abnormality. Furthermore, in
bleeding secondary to a Meckel’s diverticulum, segmental resection
is recommended because the ulcer is commonly on the mesenteric
side of the ileum, sometimes downstream of the diverticulum. Some
authors advocate for appendectomy at the time of operation for a
symptomatic Meckel’s diverticulum so as to avoid diagnostic dilemmas in the future.
Meckel's
diverticulum
FIG. 2 Technetium-99m pertechnetate scintigram from a child with a
Meckel’s diverticulum clearly differentiated from the stomach and bladder.
(From McKenzie S, Evers BM. Small intestine. In: Townsend Jr CM, ed. Sabiston
Textbook of Surgery. 19th ed. Philadelphia: Elsevier; 2012.)
children, volvulus and intussusception can occur, whereas these are
rare in adults. Symptoms are similar to non–Meckel’s-related small
bowel obstruction. Diagnosis can be made by CT scan, but often it is
made at exploration.
Bladder
Diagnosis and
Management of
Motility Disorders of
the Stomach and Small
Bowel in the Current
Era
Omar M. Ghanem, MD, and Michael G. Sarr, MD
INTRODUCTION
Unlike in the duodenal ulcer/vagotomy era of the 1950s–1980s,
motility disorders of the upper gut are currently quiteuncommon.
When present, this spectrum of disorders is difficult to both diagnose and treat effectively. To suspect these disorders,it is necessary to
understand the overall control of motility of the stomach and small
bowel; thus, we will present a very brief review of the physiology of
motility.
S u g g e S t e d R e a d i n g S
Cattell RB, Mudge TJ. The surgical significance of duodenal diverticula. N
Engl J Med. 1952;246(9):317–324.
Darlington CD, Anitha GF. Meckel’s diverticulitis masquerading as acute pan-
creatitis: a diagnostic dilemma. Indian J Crit Care Med. 2017;21(11):789–
792.
Longo WE, Vernava AM. Clinical implications of jejunoileal diverticular
disease. Dis Colon Rectum. 1992;35(4):381–388.
Makris K, Tsiotos GG, Stafyla V, Sakorafas GH. Small intestinal non-Mecke-
lian diverticulosis. J Clin Gastroenterol. 2009;43(3):201–207.
Yaqub S, Evensen BV, Kjellevold K. Massive rectal bleeding from acquired
jejunal diverticula. World J Emerg Surg. 2011;6(1):17.
Zani A, Eaton S, Rees CM, Pierro A. Incidentally detected Meckel’s diverticu-
lum: to resect or not to resect?. Ann Surg. 2008;247(2):276–281.
In brief, the contractile activities of the stomach and small intestine are controlled by the enteric (autonomic) neuromuscular system
in the wall of the gut. This is important to remember, because the
extrinsic innervation to the gut (parasympathetic/vagal nerves and
sympathetic/paravertebral nerves) do not control or initiate motility;
but rather, they can only influence motor patterns as can some hormones. Basically, contractile activity is generated by spontaneously
active neuromotor cells within the wall of thegut. When the stomach and small intestine are completely separated from the central
nervous system (as after a small intestinal transplantation),relatively
normal motility still occurs.
Contractile activity has two basic patterns, one duringfasting (the
so-called interdigestive period) and another after feeding (the postprandial period). Also, all contractile activity is oriented in a distal,
downstream direction of propagation that leads to distal transit of
ingestedfoods.
The stomach and small intestine, however, do differ in their
contractile patterns. During the interdigestive period when there is
no food ingested, the stomach and small intestine cycle through a
recurrent pattern of intense contractions that travel peristaltically
but only up to about 30 cm; this band of contractions begins in the
stomach and then moves slowlydown the small intestine over about
90 minutes. These contractions are of very high amplitude to clear
the lumen of undigested food and debris. In contrast, during the
postprandial period after ingestion of food, the contractile patterns
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maximize contact of ingested foodstuffs with the mucosa. In the
stomach, the contractile pattern mixes and mechanically breaks
down (triturates) the bigger food particles to maximize digestion
(indeed, larger food particles do not leave the stomach during
this period, because the so-called antropyloric pump controls the
size ofthe pylorus to only allow food particles <1 cm to leave the
stomach), while the small intestine slows transit through the gut to
maximize absorption.
Although we talk about “peristalsis” of the gut, the contractions
of the stomach and small intestine do NOT peristalse as does the
esophagus, where a contraction that starts in the proximal esophagus
propagates down the entire length of the esophagus in a very orderly,
peristaltic fashion (indeed the motor activity of the esophagus is
designed only to transport food into the stomach). In contrast, the
stomach and thesmall intestine are designed to move content distally
but in doing so to maximize digestion and absorption.
Contractile activity of the stomach differs considerably from the
esophagus, and understanding these differences is absolutely crucial
to diagnose gastric motility disorders. The proximal and distal stomach have different contractile activity with the proximal stomach
controlling emptying of liquids and the distal stomach the emptying
of solids. The proximal stomach has a nonphasic, slow continuous
tonic activity thatgradually relaxes the proximal stomach increasing
its volume for the ingestionof food, the so-called vagally mediated
“receptive relaxation” that allows that full plate of spaghetti we eat
to enter the large volume reservoir of the proximal stomach. Later,
the proximal stomach slowly contracts tonically, thereby decreasing
the volume reservoir, increasing intraluminal pressure, and leading
to gastric emptying of liquids. In contrast, the mid to distal stomach
has definite physic contractions (2–4 per minute) that arise froma
pacemaker region in the mid stomach (similar in principle to the
pacemaker in the heart). These contractionsthen propagate in a peristaltic manner distally from the distal mid stomach to the antrum and
down to the pylorus. Why is this important to understand? Nearly all
current motility disorders of the stomach are related to injuries of the
vagus nerves that control both the relaxation of the proximal stomach
(emptying of liquids) as well asmodifying the coordination of contractions of the distal stomach with the pylorus (emptying of solids).
The small bowel also has a pacemaker region in the proximal
duodenum that drives the rate and distal direction of contractions
in the small bowel. But peristalsis as we know it in the esophagus is
NOT present in the small bowel despite our use of the term “peristalsis” of the small bowel. Although contractile activity is phasic (6–12
per minute) and always oriented distally, the length over which a true
peristaltic contraction migrates after a meal is only 5 to 10 cm, leading to the small areas that tend to move content distally but only for
a short distance; this pattern of contractions leads to a segmenting
appearance that we readily see on contrast fluoroscopy. This pattern
increases contact of luminal content with the mucosa, slows transit, and increases absorption. Control of this activity is not vagally
dependent,but the sympathetic system does have modulatory effects
(primarily inhibitory) on small intestinal contractions as evidenced
both by postoperative ileus(POI) and especially by the condition of
adynamic ileus that can occur with retroperitoneal trauma, infection,
or “irritation.” (We will expand on this later.)
In summary, most true gastric motility disorders that currentlyoccur are related to inadvertentoperative injury to the vagus
nerves or vagal neuropathies,whereas small intestinal motility disorders are much less common and are related either to congenital/
hereditary abnormalities in the enteric nervous system or to sympathetic neural effects.
MOTILITY DISORDERS OF THE STOMACH
In our current era, objective dysmotility of the stomach (with either
documented delayed gastric emptying or dumping with accelerated
gastric emptying) occurs more typically after upper gut operations
that purposely or inadvertently cut or injure the vagus nerves or
occur as a result of damage to the vagus nerves (neuropathy) from
chronic illness, such as poorly controlled diabetes. Surgeons see
gastric dysmotility most often after operative interventions that
disrupt vagal nerve function, such as after a gastrectomy, after an
esophagectomy that necessitates transection of the vagus nerves, or
after a hiatal herniorrhaphy that injures the branches of the vagus
nerves at the esophageal hiatus. In the past when duodenal ulcer
operations centered around a truncal vagotomy, the loss of vagally
mediated receptive relaxation of the proximal stomach leads to rapid
emptying of liquids leading to dumping syndrome and/or disruption
of emptying of solids. Less commonly, after creating a Roux-en-Y
limb to drain the gastric remnant or the esophagus, gastric emptying
can be delayed. The obligate transection of the jejunum disrupts
myoelectric continuity (which controls orderly coordination of contractions) of the Roux limb with the duodenal pacemaker; this leads
to erratic, noncoordinated contractions in the Roux limb with some
contractions actually going upstream, thereby delaying gastric emptying (the so-called Roux stasis syndrome). There is also a spectrum
of idiopathic gastroparesis syndrome that usually occurs in young
females that is poorly understood and is often not associated with
any objective delay in gastric emptying; yet because of the symptoms,
this has been termed “gastroparesis-like syndrome.” Overall, true
gastric motility disorders involve either delayed emptying (mild or
severe gastroparesis) or too rapid emptying (dumping).
When functioning normally, the proximal stomach is responsible
for vagally mediated relaxation (receptive relaxation) to accommodate the entry of solids and liquids by providing a reservoir necessary
for temporary storage and the start of enzymatic and mechanical
breakdown of the ingested content. This relaxation is mediated by
the vagus nerves. In addition, some protein and fat digestion in the
stomach begins by way of pepsin and hydrochloric acid; the presence
of amino acids in the duodenum will lead to hormonal signaling
that causes a slow tonic contraction of the proximal stomach. This
tonic contraction increases the intraluminal pressure in the proximal
stomach, thereby leading to emptying of chyme into the duodenum.
In contrast, fats in the duodenum can slow gastric emptying by prolonging the relaxation of the proximal stomach. Gastric emptying
mediated by the enteric nervous system can be disrupted by surgical
procedures as previously listed. Little is known about specific causes
that lead to altered gastric emptying after gastroesophageal surgery,
but it appears to be multifactorial. The surgical process itself, in
addition to patient-related factors, such as the presence of diabetes,
hypothyroidism, chronic narcotic use, or cancer, can contribute to
this process. As aging occurs, the rate of gastric emptying decreases,
so older patients are more susceptible to this syndrome. This section
focuses on motility disorders after surgical interventions, postsurgical gastroparesis syndrome, and rapid gastric emptying. There is also
a separate section on gastroparesis-like syndrome.
Delayed Gastric Emptying/True Gastroparesis
Although uncommon, delayed gastric emptying can occur after
operations on the distal esophagus or stomach that include a known
or inadvertent vagotomy, Roux-en-Y gastrojejunostomy, or even after
an antireflux procedure. The risk of delayed gastric emptying after a
gastrectomy that includes a truncal vagotomy increases twofold and
can plague patients undergoing a classic pancreatoduodenectomy
(which includes an antrectomy) with the Roux-en-Y reconstruction
with a rate of up to 30%. The exact causes are unknown, but certainly
vagus nerve dysfunction is a key contributor as is the disruption of
the continuity of the proximal jejunum with the duodenal pacemaker
after duodenal resection leading to incomplete emptying or gastric
stasis. Truncal vagotomy causing the disruption of afferent vagal
signaling to the brain also may lead to stasis or even gastric atony.
Clinical Presentation and Diagnosis
Symptomatically, patients found eventually to have an objective
delay in gastric emptying (i.e., true gastroparesis) and not the
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gastroparesis-like syndromes (see later, Gastroparesis-Like Syndromes) often describe epigastric fullness or pain and complain of
early satiety that may or may not be accompanied by nausea and
vomiting, usually of solids more than liquids. Look for delayed
vomiting of undigested food, hours or even the day after ingestion of
the solid food; this delayed vomiting of undigested food is virtually
pathognomonic of gastroparesis provided there is no mechanical
gastric outlet obstruction. Liquid intake will be better tolerated than
solids but may be limited by early satiety, anorexia, or the inability to
ingest enough calories because of symptoms of gastric fullness; this
situation can be severe enough that patients may develop dehydration, weight loss, or malnutrition.
A detailed history is necessary to evaluate risk factors, such as
prior upper abdominal surgery (esophageal, gastric, or duodenal),
or metabolic disturbances, such as diabetes or rarely hypothyroidism. The physical examination is often not helpful, but a succussion
splash will be evidence of delayed emptying of the stomach but most
probably from a mechanical obstruction. During the diagnostic
phase, it will be necessary to exclude any type of mechanical obstruction, such as an efferent limb syndrome, anastomotic stricture, or
rarely an intussusception after a gastroenterostomy. Once mechanical obstruction is excluded, clinicians must exclude metabolic
derangements that can be observed from persistent vomiting or contributing causes, such as diabetes and hypothyroidism. It is important to evaluate the nutritional state with nutritional parameters such
as serum albumin levels. Because albumin levels may be normal
(they take a week or more to decrease substantially), ordering a prealbumin that has a shorter half-life may help determine a more acute
or subacute process. If patients have a mechanical obstruction at the
gastroenteric anastomosis identified as an anastomotic stricture or a
stricture immediately downstream from the anastomosis, ensure that
they are not abusing aspirin or nonsteroidal antiinflammatory drugs
(NSAIDs) and thereby contributing to ulceration and anastomotic
inflammation. Unfortunately, patients will not always admit this, so
if you suspect it, check a urinary level of aspirin, not a serum level
that is more transient.
Imaging can begin with abdominal x-rays with contrast to rule
out a mechanical obstruction. One caveat to remember: most cases
of a gastric motility disorder leading to gastroparesis do NOT have
gastric distension, because as stated earlier, most cases are related to
vagal dysfunction and the loss of proximal gastric relaxation; there
may, however, be solid matter retained in the remnant. In contrast, if
there is a markedly dilated gastric pouch of stomach, it is much more
likely due to a mechanical obstruction. One exception is the transient
POI or a generalized adynamic ileus in which the stomach may very
well be distended.
Upper endoscopy will allow visualization of undigested food in
the stomach (always an abnormal sign if present more than 2 or
at most 3 hours after ingestion), elimination of the possibility of
anastomotic stricture, and the means by which to obtain biopsies if
necessary. Remember, postvagotomy gastroparesis and most other
forms of gastroparesis are NOT associated with a dilated, distended
stomach.
Currently, there are three potential tests to demonstrate delayed
gastric emptying objectively: scintigraphy, wireless motility capsule
(WMC), and carbon breath testing. The gold standard for evaluation
of delayed gastric emptying, and thus the diagnosis of gastroparesis,
is the 4-hour scintigraphic gastric emptying of solids. The most
reliable parameter for the diagnosis is gastric retention of solids is
based on the percent retention at 4 hours, graded as mild (<15%),
moderate (16%–35%), and severe (>35%) gastroparesis. The WMC,
though new and a technique that avoids the (minimal) radiation
exposure of a scintigraphic technique, is not well standardized and
relies on the emptying of just this one capsule; this test is used primarily under experimental studies. Carbon breath testing has been
used in Japan and elsewhere but is still experimental in the United
States and is not used except in selected centers. Barium swallow is
not a good measure of gastric emptying, and gastric manometry,
when available, has not really become a go-to diagnostic test. With
the presence of retained solid food in the gastric reservoir, these
studies attempting to quantify the rapidity of gastric emptying are
usually not necessary.
Nonoperative Treatment
Treatment begins with the management of contributing factors, such
as obtaining tighter glucose control or treatment of hypothyroidism.
The mainstay of treatment is directed at modifying the diet. One
should focus on encouraging the ingestion of liquids more than
solids and adapting to smaller and more frequent meals (ideally six
or even more if necessary while awake). If well-tolerated, some of
the high-calorie, high-protein, low-fat, so-called small particle liquid
formulations, though often not as palatable, can provide the necessary calories for patients with nutritional challenges; if associated
dumping (see later) is problematic, the high-calorie liquids may not
be a good option, but the high-protein formulations may help. The
authors recommend a low-residue diet (i.e., lower fiber content) and
softer foods that do not require mechanical breakdown. Remember,
this will be the mainstay of treatment. Having the patient develop a
relationship with an informed dietician can be extremely beneficial.
Pharmacologic agents: If dietary modification does not manage
symptoms, a trial of a prokinetic drug, such as metoclopramide,
domperidone (if the patient still has an antrum, which is where
domperidone takes effect), or low-dose erythromycin (125 mg) that
activates the prokinetic motilin receptor, may help stimulate emptying, but NOTE not the usual antibacterial doses of 250 or 500mg
(Table 1). Be aware that these medications do not work in most
patients, and if after a short trial no results occur, there is no benefit
of continuing their use. The medications used most commonly are
metoclopramide and domperidone. As with any D2 receptor antagonist that penetrates the blood-brain barrier, extrapyramidal side
effects can occur. Metoclopramide should be started at 5 to 10 mg
three times daily but needs to be administered 30 minutes before
each meal; the use of >40 mg per day is associated with a not-insignificant risk of extrapyramidal effects, both acute (spasmodic
dystonias) and chronic (tardive dyskinesia), especially in the elderly.
As the prescribing physician, you will need to explain and warn
patients of this very alarming side effect and stop the medication
if any such symptoms occur. The latter risk has led to the US Food
and Drug Administration (FDA) to issue a black box warning that
has effectively decreased its use as an antinausea medication as well
as a prokinetic agent. Domperidone, although not approved in the
United States, is a closely related D2 receptor antagonist that does
not cross the blood-brain barrier. This agent is used widely outside
the United States and still is recommended frequently by US physicians (with patients obtaining this medication from other countries
such as Canada). Recently, however, concerns about cardiovascular
proarrhythmic risks (QT prolongation and tachyphylaxis) are the
most concerning adverse effects from domperidone that has led to
warnings in Europe and has had some feedback in the United States.
Erythromycin is useful for improving gastric emptying in the short
term (e.g., in hospitalized patients) but has never been rigorously
evaluated for symptomatic relief with its long-term use; its tachyphylaxis requires “drug holidays.”
Several newer, highly selective 5HT3 antagonists and 5HT4
receptor agonist medications may help selected patients with the
nausea and vomiting, but do not expect these agents to increase
effective gastric emptying. Total parental nutrition (TPN) or, if tolerated, enteral nutrition may be required in severe and life-threatening
cases of malnutrition; indeed, enteral delivery of nutrition should
always be tried before TPN. Finally, tricyclic antidepressants have
been suggested and may be considered for especially refractory nausea and vomiting, but the data are quite controversial, because the
anticholinergic component of it could potentially worsen symptoms
and it might actually retard gastric emptying. Therefore, these agents
should be considered only with close monitoring and only after failure of prokinetic agents.
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TABLE 1 Medications for Gastroparesis
Drug Indication Mechanism Dose Side Effects
Metoclopramide Gastroparesis (FDA-
approved for this
indication)
Domperidone Gastroparesis (not avail-
able in the United States
except under FDA IND);
often can be bought in
Canada
Erythromycin Gastroparesis (off-label) Motilin receptor agonist
Mirtazapine Gastroparesis (off-label) Alpha adrenergic, 5HT2,
Prucalopride Gastroparesis POI, CIIPO
(off-label)
Central/peripheral dopa-
mine receptor antagonist,
5HT3 receptor antagonist, 5HT4 receptor
agonist (prokinetic and
antiemetic)
Peripheral dopamine recep-
tor antagonist (prokinetic and antiemetic)
(prokinetic)
5HT3, and H1 receptor
antagonist (prokinetic,
antiemetic)
Highly selective 5HT4
receptor agonist (prokinetic, secretagogue)
5–10 mg 3 times daily
30 min before meals
10–20 mg 4 times daily Rarely can cause QTc
50–125 mg given 30 min-
utes before a meal; note
the dose is considerably
less than that used for an
infection
15–30 mg
every day at bedtime
1–2 mg daily Headache, nausea, abdomi-
Up to 30% CNS symptoms
to some extent: most
serious is Parkinsonian,
tardive dyskinesia (FDA
black box warning)
prolongation, with
risk of arrhythmia;
hyperprolactinemia
May worsen nausea, vom-
iting, abdominal pain;
tachyphylaxis with longterm use requires drug
holidays; can cause QTc
prolongation with risk of
arrhythmia, greater doses
can cause vomiting and
nausea
This is an antidepressant,
can cause somnolence,
increased appetite, and
weight gain
nal pain, diarrhea
CIIPO, Chronic idiopathic intestinal pseudo-obstruction; CNS, central nervous system; FDA, US Food and Drug Administration; GI, gastrointestinal;
IND, investigational new drug; POI, postoperative ileus.
Operative Treatment of Delayed Gastric Emptying
Operative intervention should be limited to patients with severe,
medically refractory symptoms affecting quality of life and challenging the patient’s nutritional health. First, we will discuss those
patients with objective evidence of delayed gastric emptying (true
gastroparesis). A jejunal feeding tube (percutaneous or open or as
one of the authors prefers a duodenostomy) may be indicated, but
only after a trial of nasoenteric feeding to evaluate for tolerance of
such feedings; NOTE: such a trial is absolutely essential, because
some patients have a poorly understood postvagotomy small bowel
dysmotility and cannot tolerate these feedings. This is especially
true for patients who also complain of substantial abdominal pain,
which is another indication that a trial of feedings is absolutely crucial before placing a J tube. The inability to tolerate enteric feedings,
either because they cannot tolerate the volume related to severe
bloating or the feedings exacerbate the abdominal pain, is a very bad
sign for the optimistic hope of a good response to enteric feedings.
In some situations of severe refractory gastroparesis, TPN may be the
only viable option. A venting gastrostomy tube may assist with the
feeling of gastric fullness or persistent vomiting; one just needs to be
careful to monitor how much volume is lost via such a gastrostomy
tube, because the volume will have to be replaced. Also, if the gastric
drainage is voluminous and bilious, loss of bile salts will be a distinct
possibility and may even require reinfusing the gastric drainage; as
might be expected, this is quite cumbersome and not at all appealing,
and thus placement of a gastrostomy tube alone may not be the best
option. If the enteric feeding trial is successful, then some form of
direct, enteric placement of a feeding tube is best. Placement can be
done either via a laparoscopic, open, or direct percutaneous placement (PEJ) rather than a PEG tube with a jejunostomy extension,
the latter of which all too often flips back up into the stomach and
requires replacement via gastroscopy.
In a small subset of patients with objective gastroparesis and who
had undergone an operation with a postoperative total vagotomy or
a defined vagal injury, a near total (>95%) gastrectomy (with a cardiojejunostomy leaving no effective volume reservoir) or even a completion gastrectomy may be an option. A multidisciplinary discussion
is mandatory before recommending this controversial strategy. An
examination of 20 years of Mayo Clinic’s experience of providing near
total or completion gastrectomy in patients with severe postsurgical
gastroparesis after a prior partial gastrectomy with truncal vagotomy
showed that only about half the patients were able to maintain their
nutrition orally. A similar trial of near total gastrectomy after a prior
Nissen fundoplication in patients with postsurgical gastroparesis who
had also had a pyloroplasty (remember the vagus nerves also help to
coordinate antropyloric function presumed to be related to vagal nerve
injury) found no benefit; the majority of this unusual subset of patients
had persistent symptoms and required supplemental nutrition (enteral
or parenteral) after the gastric resection. Please Note! We learned early
on that a trial of enteric feedings was absolutely necessary with any type
of operative intervention designed to deliver food by mouth, because
as stated before, if the patient cannot tolerate enteric feedings, then the
delivery of ingested foods into the jejunum via the esophagus will also
not be tolerated. Therefore, the authors do not recommend near or total
gastrectomy as a routine strategy for postsurgical gastroparesis, except
in selected patients who are demonstrated to tolerate enteric feedings.
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In recent years, there has been a new interest in various stomach-specific treatments that might appear to help with gastric
emptying, including pyloroplasty, either done as a formal operation
(laparoscopic or open) or via an endoscopic approach titled per-oral
pyloromyotomy (POP) or gastric per-oral endoscopic myotomy
(G-POEM; also known as POEM or endoscopic POP) based on
the rationale that pyloric dysfunction could result in gastric outlet
obstruction. If any of these procedures are to be considered, a preoperative trial of injection of botulinum toxin into the pylorus should
be considered strongly. This temporizing approach relaxes the pylorus similar to a pyloroplasty; if no symptomatic relief occurs, then an
operative procedure on the pylorus is probably not indicated. Sleeve
gastrectomy (with or without pyloroplasty) has received quite a bit of
interest recently. This operation decreases the reservoir capacity of
the stomach because it resects all the fundus and the lesser curvature
tube has no substantial reservoir capacity; when combined with a
pyloroplasty, there should be no resistance at the pylorus, and thus
there is some theoretic interest in its potential efficacy. The operation
might increase gastric emptying and thus have an emerging role in
the treatment of gastroparesis, especially in patients suffering from
obesity and/or diabetes. The data are still scarce and not yet well
accepted, and gastroesophageal reflux disease in the setting of a
sleeve anatomy and nonresolving gastroparesis remain of concern
without even midterm postoperative data. Acupuncture has been
shown anecdotally to have some symptomatic benefit in the management of selected patients with gastroparesis.
Finally, implantation of an electrical gastric stimulator (Fig. 1)
into the stomach wall has been suggested with increasing frequency
by some groups; this approach of gastric electrical stimulation (GES)
may be an option for patients with severe and refractory gastroparesis and who have diabetes or with predominant symptoms of
nausea or vomiting. Although these nerve stimulators might help
with nausea and vomiting, they are very controversial, with quite
radically different success reported by various groups. Because
GES does not reliably increase effective gastric emptying (see later,
Gastroparesis-Like Syndromes), be aware that patients may consider
these like a cardiac pacemaker that will “pace” the stomach and
10 cm
5-mm trocar
5-mm laparoscope
FIG. 1 Laparoscopic approach for gastric electrical stimulator:
placement of gastric wall electrodes and subcutaneous battery.
(Modified from Ginsburg GG, etal. Clinical Gastrointestinal Endoscopy. 2nd ed.
Philadelphia: Saunders; 2012.)
Subcutaneou
pocket
increase the rate of contractions, but no one has been able to show
that gastric stimulation can actually “pace” the stomach.
GASTROPARESIS-LIKE SYNDROMES
In recent times, symptoms suggestive of gastroparesis but often
without any objective delay in gastric emptying have received considerable attention in the literature. It remains unknown whether
these syndromes have always been present or whether this spectrum
of disorders are related to a more focused, increased interest in symptomatic functional disorders without objective evidence of delayed
gastric emptying. These syndromic conditions present with early
satiety, nausea, and often vomiting, mimicking true gastroparesis and
are most often seen in young females in their 20s or 30s. Although
gastroparesis by definition implies a delay in gastric emptying, it has
become clear that there is poor correlation between the severity of
delay and symptoms in these patients. A substantial percentage of
these patients have normal emptying, although their symptoms are
indistinguishable from those in patients with overt delay; this syndromic presentation is likely part of a clinical spectrum that has been
termed chronic unexplained nausea and vomiting or gastroparesis-like
syndrome. In these patients, other mechanisms (e.g., impaired gastric
accommodation with increased tension in the proximal stomach
wall, sensitization of vagal afferent pathways, etc.) may account for
the symptomatology.
Symptomatic treatment for this spectrum of complaints first
revolves around excluding true gastroparesis, often requiring a
formal radionuclide gastric emptying study. Because there is little
association of symptoms with the rate of gastric emptying, the focus
on these patients is to treat the symptoms of nausea and vomiting.
Some modification of diet as for true gastroparesis can help, but
treatment begins with antiemetics and antinausea medications. The
usual approach is to start with the classic antinausea medications,
like metoclopramide or the 5HT3 receptor antagonists, typically
beginning with ondansetron (which is also available in an orally
disintegrating tablet form) or granisetron, which is available as a
subcutaneous delivery patch. A more general approach to nausea has
been in the form of neuromodulators (e.g., tricyclic antidepressants
such as nortriptyline). Although most of these agents have prominent anticholinergic activity, these drugs generally do not affect
motility when used in low doses. Several anecdotal reports suggested
substantial relief, but a randomized controlled study showed no
improvement in nausea. A more promising agent is mirtazapine,
which is being used increasingly to treat nausea (due to its 5HT3
receptor antagonism), improve appetite, and to a lesser extent modulate functional pain. Buspirone is an anxiolytic that is an agonist of
the 5HT1A receptor, which may also be responsible for its ability to
improve gastric accommodation. It may prove useful in patients with
prominent early satiety.
Over the past 15 to 20 years, the still not fully accepted treatment
of neuromodulation by various forms of GES has been recommended with increasing frequency. GES is a technique in which
serosal electrodes are implanted onto the gastric antrum via an open
or laparoscopic approach (see Fig. 1). The accepted use for GES
includes the indication approved by the US FDA of “drug refractory disease,” but there are no defined criteria for the diagnosis of
this condition. Because under the FDA statute for the Practice of
Medicine, any FDA-approved device can be used off-label with an
adequate justification, GES can be used in the “off-label” setting.
Because the current devices for GES require a Humanitarian Use
Device (HUD) approval, any centers employing these devices should
have some form of Institutional Review Board (IRB) oversight. Some
investigators have advocated that multiple uses of GES are allowed
under certain conditions. Randomized crossover trials have shown
no or only modest symptom relief with the device when on versus
off, although many prospective, open label trials have rather aggressively suggested impressive benefit, particularly in patients with
diabetic gastroparesis. Putative mechanisms of action are presumed
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to be via modulation of vagal signaling and not via improved gastric
emptying. The bottom line is that the role of GES in gastroparesis,
despite its now relatively frequent use, remains unclear.
The problems with this spectrum of gastroparesis-like syndromes
are that we do not understand their etiology, it appears to be in
the spectrum of functional disorders of the gut, and the response
to different medications varies considerably. These patients are
best managed by a thoughtful, considerate, and understanding
gastroenterologist.
DIABETIC GASTROPARESIS
Diabetic gastroparesis should be discussed as a separate entity. Most
investigators agree that this disorder is related primarily to poor glucose control and its effects on vagal nerve function. One important
aspect of this disorder is that although it is associated with a true
delay in gastric emptying, the clinical symptomatology waxes and
wanes in severity, and thus any attempt to intervene in an irreversible
way is usually to be avoided. Many times, the symptoms are more
cumbersome than any problems with caloric intake or nutrition
aside from the underlying diabetes mellitus.
This intermittent nature of diabetic gastroparesis should weigh
into any therapeutic considerations. Attempts to obtain better control of glucose intolerance are definitely appropriate. Some reports
suggest that the use of insulin pumps in patients with type 1 diabetes
can lead to fewer hyperglycemic events, a decrease in HbA1c, and
considerable improvement in the symptoms of gastroparesis. Of
course, the initial therapeutic suggestions should concentrate on
dietary modifications as discussed earlier and trying the various
pharmacologic agents as for other forms of gastroparesis. A true
venting gastrostomy may be advantageous in these patients for relief
from bloating symptoms, but as with any gastrostomy, it should not
be open to continuous drainage for fear of dehydration, bile salt wasting, and so on. Specific counseling of patients with such a venting
gastrostomy is imperative. Also, this may be a potential avenue for a
somewhat safer jejunal extension tube to allow intrajejunal feedings
if the patient can tolerate them. In terms of a gastric resection, the
senior author of this chapter performed a near total gastrectomy in
one highly unusual patient with chronic, unrelenting diabetic gastroparesis of 5 years’ duration who could also tolerate jejunal feedings.
Although this patient did well for 8 years after which follow-up was
lost, we want to stress that this approach (tailored after treatment of
vagal dysfunction in selected patients as described before) should not
be considered in the overwhelming majority of patients with diabetic
gastropareses.
Because diabetic gastroparesis can lead to considerable symptomatology of vomiting and nausea, GES might have benefit in this
population and should be entertained in the highly symptomatic
patient. Whether it will augment gastric emptying is not necessarily
to be expected, but it may help with symptoms.
RAPID GASTRIC EMPTYING
The overly rapid early emptying of gastric contents from the stomach into the duodenum or the jejunum, also known as dumping,
can result from gastric operations that almost universally involve a
vagotomy; this condition leads to the dumping of a bolus of liquid
or hyperosmolar chyme into the proximal gut. Approximately 10%
to 15% of patients experience some extent of dumping after gastric
surgery. If the contents are of high osmolarity, such as a carbohydrate-rich bolus, then the resultant symptoms can be very unpleasant
for the patient. Because of increased osmolality, some have suggested
that the rapid shift of fluid into the lumen of the small bowel can
lead to feelings of bloating. The old theory that dumping may result
in a relative hypovolemia from the fluid shift into the gut has been
disproven and is not the primary cause of the symptoms; indeed,
the majority of the symptoms arise from the release of vasoactive
substances related to the high osmolality of the intraluminal content.
Also important to remember is that many physicians relate dumping
to diarrhea; this is neither appropriate nor accurate, because many
patients with dumping have no diarrhea. The symptoms of dumping
are abdominal bloating, nausea, and the feeling of a need to lie down
early after eating; diarrhea may occur but not always.
Dumping can be seen after virtually any operation on the distal
stomach but usually those involving a vagotomy; the greatest frequency is after subtotal gastrectomy with vagotomy and the least
frequent is after pyloroplasty alone. Patients who have undergone
a truncal vagotomy (or an inadvertent or necessary vagotomy) and
pyloroplasty will experience dumping at greater rates than those who
had pyloroplasty alone. The symptoms occur early, usually within
30 minutes of eating. Symptoms are likely to be elicited after a large,
rapidly ingested meal and are much worse with liquid meals of high
osmolarity. In the past, dumping was a very common feature after
truncal vagotomy and pyloroplasty, but in the current era, dumping
is observed primarily after Roux-en-Y gastric bypass surgery. Thankfully, dumping rarely is a permanent state, especially after gastric
bypass, in which the majority of patients will not have prominent
or persistent symptoms after the first 3 months. Predicting who will
develop dumping is challenging.
There is also a form of dumping called late dumping, in which
the symptoms occur 90 minutes to 3 hours after eating. This symptomatology is believed to be related to the delivery of high-calorie
meals to the more distal intestine, whereby a different neurohormonal milieu occurs. The initial symptoms are quite similar to early
dumping, but also often involve diarrhea, which is not a part of early
dumping. Some of the symptomatology of this late dumping appear
to be related to the entry of high caloric value into the duodenum
or jejunum overwhelming the regulatory mechanisms for insulin
release, resulting in a delayed continuous increase in the levels of
serum insulin leading to the rapid “reactive” development of hypoglycemia; this rapid onset of hypoglycemia then causes symptoms
very similar to early dumping along with the symptoms of hypoglycemia. Indeed, the hypoglycemia can be quite severe (<20 mg/dL)
and can even lead to disturbed thinking, seizures, and even coma.
Although some have described this late hypoglycemia as a new
postbariatric syndrome called noninsulinoma postprandial pancreatogenous hypoglycemia syndrome (NIPPS) that can occur after a
Roux-en-Y gastric bypass, quite frankly, this syndromic complex was
well-recognized in the past era of duodenal ulcer operations as “late
dumping” after gastric resections.
Clinical Presentation and Diagnosis
The majority of patients, about 75%, will present with early rather
than late symptoms of dumping. The differential diagnosis must
exclude the afferent loop syndrome, pancreatic insufficiency, and
bowel obstruction after prior gastric surgery. A detailed history will
help to differentiate between dumping and these other potential
complications. With early dumping, patients will complain of early
satiety, abdominal pain, nausea, and evidence of autonomic dysfunction, such as a racing heartbeat, sweating, dizziness, and tremors.
Unlike with late dumping, diarrhea is not common with early dumping symptoms. The symptoms may last for about an hour, because
the high osmolarity causes release of vasoactive substances. Patients
often are self-immobilized and want to lie down because of the
severity of the ill feeling they experience. Late dumping has similar
symptoms but generally occurs approximately 90 minutes to 3 hours
after a meal. Additional features include fatigue, mental changes, or
even fainting associated with reactive hypoglycemia. Recognition of
this unfortunate sequela is important for patients to understand so
that they can seek appropriate care if needed.
Provocative testing to help confirm the diagnosis of late dumping
involves giving 50g of orally administered glucose followed by serial
measurements of glucose and plasma insulin levels as well as heart
rate and determining any symptoms of dumping experienced by
the patient. Some suggest a concomitant, hydrogen breath test; an
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increase in the heart rate greater than 12 beats per minute and an
increase in hydrogen breath excretion allegedly has a sensitivity of
94% and a specificity of 92%. An upper gastrointestinal (GI) series
may help to define anatomy but is often not necessary. Usually,
however, the diagnosis is evident by the patient’s symptoms and the
clinical setting.
Treatment
The primary treatment of dumping syndrome is dietary modification. Avoiding simple sugars (which includes alcohol and most
dessert-type food items) and the intake of calorie-dense carbohydrates helps minimize symptoms. Simple measures, such as avoiding
drinking 30 minutes before, during, and after a meal also may help.
Adding fiber supplements and complex carbohydrates may help to
slow transit; in addition, drinking plenty of water at other times
during the day, especially if concomitant diarrhea is present, serves
to avoid dehydration as a result of the dumping. Patients should
avoid an upright posture while eating and instead recline if possible
after eating, because upright posture may accelerate gastric emptying in some patients. Although diarrhea is not the main presenting
symptom of dumping, patients may have a late onset of diarrhea. As
before, eating small, frequent meals and having proteins and fats with
meals may help to slow gastric emptying.
Dietary modifications alone may not relieve the dumping symptoms; 3% to 5% of patients will have refractory symptoms. A trial
of octreotide in these patients may offer great relief of the dumping
symptoms but in only about 20% of patients. In several randomized,
controlled trials, octreotide improved symptoms in some patients
when compared with controls. If octreotide is effective, then a longer-acting formulation of octreotide should be used. The timing of
administration of subcutaneous octreotide is important and should
be given 30 minutes before a meal. For patients on long-acting octreotide, steatorrhea can be a problem, because octreotide inhibits
pancreatic enzyme secretion, but the resulting steatorrhea can be
ameliorated with pancreatic enzyme replacement. Increasing the
viscosity of the intraluminal contents by adding pectin and guar may
slow the emptying process and alleviate symptoms.
The role of any operative interventions to manage dumping is
limited. Distant literature describes the use of a 10-cm, reversed
jejunal limb at 100cm distal to the ligament of Treitz in patients
who have severe diarrhea associated with rapid gastric emptying.
There are, however, many complications with these reversed limbs,
and studies have not shown any substantial benefit; this often
quoted but outdated procedure should be relegated to history and
no longer used currently. For the late form of dumping and the
hypoglycemia associated with Roux-en-Y gastric bypass (NIPPS),
endoscopic transoral outlet reduction (TORe) might be of benefit in
some patients. With this procedure, the diameter of the gastrojejunostomy is decreased via endoscopic suturing, but consistently good
results across different practices are lacking. Operatively reversing
the gastric bypass or redirecting the Roux limb into the duodenum
may be the only option. A prior high visibility suggestion of subtotal
pancreatectomy to treat any associated hypoglycemia has proven to
be ineffective in long-term outcomes.
MOTILITY DISORDERS OF THE SMALL
INTESTINE
True motility disorders of the small intestine are actually quite
unusual and represent a spectrum from transient, reversible problems of motility, such as generalized adynamic ileus to the rare
and progressive familial disorders of chronic idiopathic intestinal
pseudo-obstruction and the acquired disorder of scleroderma.
There are also several unique, albeit rare, clinical scenarios that
involve motor abnormalities, such as the bypass enteropathy of the
defunctionalized jejunoileum in patients after the original bariatric
operation of the jejunoileal or “small bowel” bypass, small intestinal
intussusception, and the dysmotility that can complicate small bowel
function in patients who were born with intestinal atresia. This section, however, will focus on the two forms of adynamic ileus and the
pseudo-obstructions of the small bowel.
Adynamic Ileus
A true small intestinal “ileus” after intraabdominal operations actually is very unusual. In contrast, the “physiologic ileus” that occurs in
the early postoperative period (first 1 to 4 days) after a laparotomy is
often talked about and called “postoperative ileus.” This form of transient ileus, or the inability to eat and have bowel movements, is primarily a gastric and colonic response to the abdominal wall trauma
of a laparotomy. Interestingly, it is not a small bowel ileus or even a
dysmotility of the small bowel; indeed, small intestinal contractile
activity is present during the operation as can be seen and demonstrated by “tweaking” the small bowel and observing it contract (in
contrast to the stomach and colon, which have no spontaneous or
stimulated contractile activity intraoperatively). Also, intraintestinal
feeding can be administered immediately postoperatively. In essence,
the small intestine works relatively normally, whereas the motor
activity leading to gastric emptying and colonic emptying is delayed
for 2 to 4 days. Thus, POI is not a small bowel dysmotility. The
absence of “bowel sounds” early postoperatively is due to the loss of
gastric emptying of swallowed gas; it is the gas/liquid interface that
leads to bowel sounds.
Adynamic ileus, however, is a rare, generalized motor disorder of
the entire gut, involving the small intestine as well as the stomach and
colon. Adynamic (generalized) ileus involves a secondary, neurally
mediated blockade of effective contractile activity in response most
commonly to a systemic inflammatory disorder (such as sepsis), after
retroperitoneal operations (e.g., kidney transplantation), or with
retroperitoneal conditions (e.g., trauma, hematoma), all believed to
interfere with the autonomic nervous innervation to the gut. True
adynamic ileus should not be confused with isolated colonic ileus
(colonic pseudo-obstruction) that can complicate a total hip arthroplasty or retroperitoneal operations; this form of localized ileus
involves only the colon but not the stomach or small bowel.
Clinical Presentation and Diagnosis
Diagnosis is based on the presence of symptoms similar to those
of a small bowel obstruction that occur in the appropriate clinical
setting: vomiting, bloating, abdominal distention, obstipation of
stool and gas, and the physical findings of tinkling bowel sounds and
generalized bowel distention (small and large bowel) on diagnostic
imaging. Crampy abdominal pain as occurs with a mechanical small
bowel obstruction, however, is distinctly unusual. With a heightened
clinical suspicion, a simple abdominal radiograph will suffice showing the dilation of the stomach, small intestine, and entire colon.
The differential diagnosis includes the exclusion of an obstructing
rectal lesion, which may require proctoscopy or a transrectal contrast
radiograph.
Treatment
Treatment should be directed at the cause of the ileus, most commonly sepsis. Specific pharmacologic or operative intervention is
neither needed nor effective in an attempt to treat or reverse the ileus.
Management is otherwise conservative, often including a nasogastric
tube. Prokinetic agents are not effective. Adynamic ileus is transient
and resolves when the systemic cause of the ileus has been controlled.
Postoperative Ileus
We want to differentiate POI from adynamic ileus; these represent
two distinct and different entities. The former is a physiologic
response to abdominal wall trauma, while the second is a pathologic
response to infection, etc. Also, to be clear, POI involves the stomach and colon but not the small intestine as stated earlier, whereas
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