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22. What is the characterization of a rolling or type II paraesophageal hernia?
A. Upward dislocation of the colon in the posterior
mediastinum
B. Upward dislocation of both the cardia and gastric
fundus in the posterior mediastinum
C. Upward dislocation of the gastric fundus in the pos-
terior mediastinum
CHAPTER 25
D. Upward dislocation of the cardia in the posterior
mediastinum
The Esophagus and Diaphragmatic Hernia
Answer: C
With the advent of clinical radiology, it became evident that
a diaphragmatic hernia was a relatively common abnormality
and was not always accompanied by symptoms. Three types of
esophageal hiatal hernia were identified: (a) the sliding hernia,
type I, characterized by an upward dislocation of the cardia in
the posterior mediastinum (Fig. 25-8A); (b) the rolling or PEH,
type II, characterized by an upward dislocation of the gastric
fundus alongside a normally positioned cardia (Fig. 25-8B);
and (c) the combined sliding-rolling or mixed hernia, type III,
characterized by an upward dislocation of both the cardia and
the gastric fundus (Fig. 25-8C). The end stage of type I and
type II hernias occurs when the whole stomach migrates up
into the chest by rotating 180° around its longitudinal axis,
with the cardia and pylorus as fixed points. In this situation,
the abnormality is usually referred to as an intrathoracic stomach (Fig. 25-8D). In some taxonomies, a type IV hiatal hernia
is declared when an additional organ, usually the colon, herniates as well. (See Schwartz 11th ed., pp. 1046–1047.)
FIG. 25-8. A. Radiogram of a type I (sliding) hiatal hernia. B. Radiogram of a type II (rolling or paraesophageal) hernia. C. Radiogram of a
type III (combined sliding-rolling or mixed) hernia. D. Radiogram of an intrathoracic stomach. This is the end stage of a large hiatal hernia
regardless of its initial classification. Note that the stomach has rotated 180° around its longitudinal axis, with the cardia and pylorus as fixed
points. (Reproduced with permission from Nyhus LM, Condon RE. Hernia, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1989.) (Continued)
BA
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CHAPTER 25
The Esophagus and Diaphragmatic Hernia
C
D
FIG. 25-8. (Continued)
23. The best treatment for a patient with a symptomatic
Schatzki ring without complaints of reflux is:
A. Antireflux surgery.
B. Excision of the ring.
C. Dilation.
D. Ablation.
E. Proton pump inhibitor (PPI).
Answer: C
Symptoms in patients with a ring are caused more by the
presence of the ring than by gastroesophageal reflux. Most
patients with a ring but without proven reflux respond to
one dilation, while most patients with proven reflux require
repeated dilations. In this regard, the majority of Schatzki
ring patients without proven reflux have a history of ingestion
of drugs known to be damaging to the esophageal mucosa.
Bonavina and associates have suggested drug-induced injury
as the cause of stenosis in patients with a ring, but without
a history of reflux. Because rings also occur in patients with
proven reflux, it is likely that gastroesophageal reflux also
plays a part. This is supported by the fact that there is less
drug ingestion in the history of these patients. Schatzki ring
is probably an acquired lesion that can lead to stenosis from
chemical-induced injury by pill lodgment in the distal esophagus, or from reflux-induced injury to the lower esophageal
mucosa.
The best form of treatment of a symptomatic Schatzki ring
in patients who do not have reflux consists of esophageal dilation for relief of the obstructive symptoms. In patients with
a ring who have proven reflux and a mechanically defective
sphincter, an antireflux procedure is necessary to obtain relief
and avoid repeated dilation. (See Schwartz 11th ed., p. 1049.)
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24. A characteristic finding on Barium swallow for eosinophilic esophagitis (EE) is:
A. Feline esophagus.
B. Apple core esophagus.
C. Bird’s beak esophagus.
D. Rat’s tail esophagus.
CHAPTER 25
The Esophagus and Diaphragmatic Hernia
FIG. 25-9. The esophagus on the left shows a stacking
of rings, demonstrating eosinophilic esophagus. The
esophagus on the right is a normal barium swallow.
Answer: A
A barium swallow should be the first test obtained in the
patient with dysphagia. EE has a characteristic finding often
called the “ringed esophagus” or the “feline esophagus,” as the
esophageal rings are felt to look like the stripes on a housecat
(Fig. 25-9). The endoscopic appearance of EE is also characteristic, and also appears as a series of rings (Fig. 25-10).
(See Schwartz 11th ed., p. 1051.)
FIG. 25-10. The endoscopic appearance of
eosinophilic esophagitis is characteristically a
series of stacked mucosal rings.
25. Patients who undergo diverticulopexy, instead of diverticulectomy, for treatment of Zenker’s diverticulum have
a lower risk of:
A. Fistula formation.
B. Hematoma.
C. Recurrent nerve paralysis.
D. Difficulties in phonation.
E. Horner’s syndrome.
Answer: A
If the diverticulum is excessively large so that it would be
redundant if suspended, or if its walls are thickened, a diverticulectomy should be performed. This is best performed
under general anesthesia by placing a Maloney dilator (48F)
in the esophagus, after controlling the neck of the diverticulum and after myotomy. A linear stapler is placed across the
neck of the diverticulum, and the diverticulum is excised
distal to the staple line. The security of this staple line and
effectiveness of the myotomy may be tested before hospital
discharge with a water-soluble contrast esophagogram. Postoperative complications include fistula formation, abscess,
hematoma, recurrent nerve paralysis, difficulties in phonation, and Horner syndrome. The incidence of the first two
can be reduced by performing a diverticulopexy rather than
diverticulectomy. (See Schwartz 11th ed., pp. 1053–1054.)
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26. Patients who present with achalasia should NOT be
offered which of the following treatment options?
A. Heller myotomy with 270o Belsey fundoplication
B. Heller myotomy with Toupet posterior 180o
fundoplication
C. Heller myotomy with Dor anterior 180o
fundoplication
D. Heller myotomy with complete 360o fundoplication
27. Clinical factors that are poor prognosticators in esophageal cancer and exclude surgery for curative intent
include the following EXCEPT:
A. Recurrent nerve paralysis.
B. Horner syndrome.
C. Persistent spinal pain.
D. Malignant pleural effusion.
E. Hematemesis.
Answer: D
The third issue—and one that has been long debated—is
the question of whether an antireflux procedure should be
added to a surgical myotomy. Excellent results have been
reported following meticulously performed myotomy without an antireflux component. Retrospective studies, with
long-term follow-up of large cohorts of patients undergoing
Heller myotomy demonstrated that, after 10 years, >50% of
patients had reflux symptoms without a fundoplication. In a
recent randomized clinical trial, 7% of patients undergoing
Dor fundoplication following lower esophageal sphincter
(LES) myotomy had abnormal 24-hour pH probes, and 42%
of patients with a myotomy only had abnormal reflux profiles.
If an antireflux procedure is used as an adjunct to esophageal
myotomy, a complete 360° fundoplication should be avoided.
Rather, a 270° Belsey fundoplication, a Toupet posterior 180°
fundoplication, or a Dor anterior 180° fundoplication should
be used to avoid the long-term esophageal dysfunction secondary to the outflow obstruction afforded by the fundoplication itself. (See Schwartz 11th ed., pp. 1055–1056.)
Answer: E
Clinical factors that indicate an advanced stage of carcinoma
and exclude surgery with curative intent are recurrent nerve
paralysis, Horner syndrome, persistent spinal pain, paralysis
of the diaphragm, fistula formation, and malignant pleural
effusion. Factors that make surgical cure unlikely include a
tumor >8 cm in length, abnormal axis of the esophagus on
a barium radiogram, more than four enlarged lymph nodes
(LNs) on computed tomography (CT), a weight loss >20%, and
loss of appetite. Studies indicate that there are several favorable parameters associated with tumors <4 cm in length, there
are fewer with tumors between 4 and 8 cm, and there are no
favorable criteria for tumors >8 cm in length. Consequently,
the finding of a tumor >8 cm in length should exclude curative resection; the finding of a smaller tumor should encourage an aggressive approach. (See Schwartz 11th ed., p. 1073.)
CHAPTER 25
The Esophagus and Diaphragmatic Hernia
28. The top three most common complications (in order of
most common to least common) following an minimally
invasive surgery (MIS) three-field esophagectomy are:
A. Pneumonia, atrial fibrillation, anastomotic leak.
B. Anastomotic leak, pneumonia, deep vein thrombosis
(DVT).
C. Atrial fibrillation, thoracic duct injury, pneumonia.
D. Pneumonia, anastomotic leak, pneumothorax.
E. Atrial fibrillation, anastomotic leak, pneumonia.
Answer: A
The MIS transthoracic two-field esophagectomy is slightly
different. In this operation, the abdominal portions of the
operation are done first, including placement of the feeding
tube, the creation of the conduit, and the sewing of the tip of
the conduit to the fully dissected gastroesophageal junction
(GEJ). The patient is then rolled into the left lateral decubitus
position and, through right thoracoscopy, the esophagus is
dissected and divided 10 cm above the tumor. Once freed, the
specimen is pulled out through the mini-thoracotomy, and
an end-to-end anastomosis stapler is introduced through the
high corner of the gastric conduit and out a stab wound along
the greater curvature. The anvil of the stapler is placed in the
proximal esophagus and held with a purse-string, the stapler
is docked, the anastomosis is created, and a gastrotomy is
then closed with another firing of the gastrointestinal anastomosis (GIA) stapler. The three-field esophagectomy has
the advantage of placing the anastomosis in the neck where
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CHAPTER 25
The Esophagus and Diaphragmatic Hernia
leakage is unlikely to create a severe systemic consequence.
On the other hand, placement of the anastomosis in the high
chest minimizes the risks of injury to structures in the neck,
particularly the recurrent laryngeal nerve. Although the leak
of the intrathoracic anastomosis may be more likely to bear
septic consequences, the incidence of leak is diminished.
Other complications of this approach relate to pulmonary
and cardiac status. In many series, the most common complication is pneumonia, the second is atrial fibrillation, and
the third is anastomotic leak. (See Schwartz 11th ed., p. 1076.)
CHAPTER 26
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Stomach
1. All of the following statements about complicated peptic ulcer disease requiring hospitalization are TRUE
EXCEPT:
A. Bleeding is the most common cause of ulcer-related
death.
B. Perforation is the most common indication for
operation.
C. Endoscopic treatment is usually effective in achiev-
ing definitive hemostasis.
D. Obstruction rarely requires operation.
2. Which of the following inhibits gastrin secretion?
A. Histamine
B. Acetylcholine
C. Amino acids
D. Acid
Answer: D
Bleeding is the most common cause of ulcer-related death,
but only rarely do patients with bleeding gastric or duodenal ulcer require operation today. The success of endoscopic
treatment and medical therapy for bleeding peptic ulcer
disease (PUD) has resulted in the selection of a small subgroup of high-risk patients for today’s surgeon. (See Schwartz
11th ed., p. 1131.)
Perforation is the second most common complication of
peptic ulcer, but nowadays it is a much more common indication for operation than bleeding. (See Schwartz 11th ed.,
p. 1134.)
Most patients with significant obstruction from chronic
ulceration will require some sort of substantial intervention.
Endoscopic balloon dilation can often transiently improve
obstructive symptoms, but many of these patients ultimately fail and come to operation. (See Schwartz 11th ed.,
p. 1136.)
Answer: D
Luminal peptides and amino acids are the most potent
stimulants of gastrin release, and luminal acid is the most
potent inhibitor of gastrin secretion. The latter effect is predominantly mediated in a paracrine fashion by somatostatin
released from antral D cells. Gastrin-stimulated acid secretion is significantly blocked by H2 antagonists, suggesting that
the principal mediator of gastrin-stimulated acid production
is histamine from mucosal enterochromaffin-like (ECL)
cells and not direct stimulation of parietal cells by gastrin.
(See Schwartz 11th ed., p. 1109.)
3. Eradication of Helicobacter pylori infection after treatment may be confirmed by all of the following EXCEPT:
A. Carbon-labeled urea breath test.
B. Serology.
C. Fecal antigen test.
D. Gastric mucosal biopsy.
Answer: B
A positive serologic test is presumptive evidence of active
infection if the patient has never been treated for H. pylori.
Histologic examination of gastric mucosal biopsy using special stains is the gold standard test for helicobacter infection.
Other sensitive tests include commercially available rapid
urease tests, which assay for the presence of urease in mucosal
biopsy specimens (strong presumptive evidence of infection).
Urease is an omnipresent enzyme in H. pylori strains that
colonize the gastric mucosa. The carbon-labeled urea breath
test has become the standard test to confirm eradication of
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CHAPTER 26
Stomach
H. pylori following appropriate treatment. In this test, the
patient ingests urea-labeled with nonradioactive 13C or 14C.
The labeled urea is acted upon by the urease present in the
H. pylori and converted into ammonia and carbon dioxide.
The radiolabeled carbon dioxide is excreted from the lungs
and can be detected in the expired air. It can also be detected
in a blood sample. The fecal antigen test also is quite sensitive and specific for active H. pylori infection and may also be
used to confirm cure after treatment. (See Schwartz 11th ed.,
p. 1117.)
Because H. pylori induces a strong immunologic response,
serological testing is useful but may not be as accurate as the
urea breath test or the stool antigen test, and a positive serology persists after eradication of H. pylori infection, so serology
is not useful to confirm successful treatment of Helicobacter
infection. (See Schwartz 11th ed., p. 1119.)
4. A patient is referred 2 years following distal gastrectomy
and Roux-en-Y reconstruction for nonhealing benign
gastric ulcer. His chief complaint is epigastric pain
relieved by vomiting undigested food. He has lost 15% of
his body weight in the past 6 months. Solid gastric emptying scan shows 20% gastric emptying at 4 hours, and
upper endoscopy is normal except for retained food in
the stomach. Treatment options include all the following
EXCEPT:
A. Transthoracic vagotomy.
B. Oral erythromycin.
C. High subtotal gastrectomy.
D. Feeding jejunostomy.
Answer: A
Gastric stasis following surgery on the stomach may be due to a
problem with gastric motor function or caused by an obstruction. The gastric motility abnormality could have been preexisting and unrecognized by the operating surgeon. Alternatively,
it may be secondary to deliberate or unintentional vagotomy, or
resection of the dominant gastric pacemaker. An obstruction
may be mechanical (eg, anastomotic stricture, efferent limb
kink from adhesions or constricting mesocolon, or a proximal small-bowel obstruction) or functional (eg, retrograde
peristalsis in a Roux limb). Gastric stasis presents with vomiting (often of undigested food), bloating, epigastric pain, and
weight loss. Once mechanical obstruction has been ruled out,
medical treatment is successful in most cases of motor dysfunction following previous gastric surgery. This consists of dietary
modification and promotility agents. (If operation is required)
gastroparesis following subtotal gastric resection is best treated
with near-total (95%) or total gastric resection and Roux-en-Y
reconstruction. (See Schwartz 11th ed., pp. 1157–1158.)
Three prokinetic (metoclopramide, erythromycin, domperidone) may be used to treat delayed gastric emptying. Typical doses and mechanism of action are shown in Table 26-1.
(See Schwartz 11th ed., p. 1115.)
5. Which of the following is secreted by gastric parietal
cells?
A. Pepsinogen
B. Intrinsic factor
C. Gastrin-releasing peptide
D. Ghrelin
E. Histamine
TABLE 26-1 Drugs that accelerate gastric emptying
Agent Typical Adult Dose Mechanism of Action
Metoclopramide 10 mg PO four times a day Dopamine antagonist
Erythromycin 250 mg PO four times a day Motilin agonist
Domperidone 10 mg PO four times a day Dopamine antagonist
Answer: B
Activated parietal cells secrete intrinsic factor in addition to
hydrochloric acid. Presumably the stimulants are similar, but
acid secretion and intrinsic factor secretion may not be linked.
Intrinsic factor binds to luminal vitamin B12, and the complex is absorbed in the terminal ileum via mucosal receptors.
Vitamin B12 deficiency can be life-threatening, and patients
with total gastrectomy or pernicious anemia (ie, patients with
no parietal cells) require B12 supplementation. (See Schwartz
11th ed., pp. 1108–1109.)
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6. The most accurate diagnostic test for Zollinger-Ellison
syndrome (ZES) is:
A. Fasting serum gastrin.
B. Computed tomography scan.
C. Endoscopy.
D. Secretin stimulation test.
Elevated serum gastrin
(off PPI + H
Measure BAO and gastric pH
RA)
2
Answer: D
All patients with gastrinoma have an elevated gastrin level,
and hypergastrinemia in the presence of elevated basal acid
output (BAO) strongly suggests gastrinoma. Patients with
gastrinoma usually have a BAO > 15 mEq/h or >5 mEq/h
if they have had a previous procedure for peptic ulcer. Acid
secretory medications should be held for several days before
gastrin measurement, because acid suppression may falsely
elevate gastrin levels. Causes of hypergastrinemia can be
divided into those associated with hyperacidity and those
associated with hypoacidity (see Fig. 26-1). The diagnosis of
ZES is confirmed by the secretin stimulation test. An intravenous (IV) bolus of secretin (2 U/kg) is given, and gastrin
levels are checked before and after injection. An increase in
serum gastrin of 200 pg/mL or greater suggests the presence
of gastrinoma. (See Schwartz 11th ed., p. 1137.)
CHAPTER 26
Stomach
BAO > 10 mEq/h
pH < 2
Secretin stimulation test
Significant elevation in serum
gastrin in response to IV secretin?
Zollinger-Ellison
syndrome
Octreotide scan
R/O MEN-1
G-cell +/or ECL
cell hyperplasia
Confirm with EGD + Bx
Consider resection
NoYes
Renal insuff
Previous GI surgery
• Vagotomy?
• Massive SB resection
Loop GJ with antral
alkalinization
Takedown GJ
Or
TV and A
BAO low
pH > 2
Antral
stasis
Consider TV
+ antrectomy
Pernicious
anemia
Confirm with EGD/Bx
test/treat H. pylori
give B
gastrectomy B
Retained antrum on
“duodenal stump”
Resect retained antrum
Convert B
12
S/P
Or
Atrophic
gastritis
2
to B
2
1
FIG. 26-1. Algorithm for diagnosis and management of hypergastrinemia. BAO = basal acid output; B1 = Billroth 1; B2 = Billroth 2; Bx = biopsy;
ECL = enterochromaffin-like; EGD = esophagogastroduodenoscopy; GJ = gastrojejunostomy; H2RA = histamine 2 receptor antagonist;
insuff = insufficiency; MEN1 = multiple endocrine neoplasia type I; PPI = proton pump inhibitor; R/O = rule out; SB = small bowel; S/P = status
post; TV = truncal vagotomy; TV and A = truncal vagotomy and antrectomy.
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7. In the patient with a secretin stimulation test suggesting
gastrinoma, which of the following is the preoperative
imaging study of choice?
A. Computed tomography (CT)
B. Magnetic resonance imaging (MRI)
C. Endoscopic ultrasound (EUS)
D. Angiographic localization
E. Somatostatin receptor scintigraphy
CHAPTER 26
Stomach
Answer: E
About 80% of primary tumors are found in the gastrinoma
triangle (Fig. 26-2), and many tumors are small (<1 cm),
making preoperative localization difficult. Transabdominal
ultrasound is quite specific, but not very sensitive. CT will
detect most lesions >2 cm in size, and MRI is comparable.
EUS is more sensitive than noninvasive imaging tests, but
it still misses many smaller lesions or lesions in inaccessible
locations (eg, the pancreatic tail). Somatostatin receptor scintigraphy (the octreotide scan) or Gallium-68 dotatate positron emission tomograph/computed tomography (PET/CT)
are sensitive and specific when the pretest probability of gastrinoma is high and may identify sites of regional or distant
metastatic disease. (See Schwartz 11th ed., p. 1137.)
8. A patient on chronic steroids and nonsteroidal antiinflammatory drugs (NSAIDs) for rheumatoid arthritis
requires operation for bleeding duodenal ulcer. Patients
like this:
A. Have a 90-day mortality risk of 5%.
B. Far outnumber patients requiring operation for per-
forated duodenal ulcer.
C. Should be considered for lifelong acid suppression if
vagotomy is omitted.
D. Are usually treated with distal gastrectomy.
FIG. 26-2. Gastrinoma triangle.
Answer: C
Bleeding is the most common cause of ulcer-related death, but
only rarely do patients with bleeding gastric or duodenal ulcer
require operation today. The success of endoscopic treatment
and medical therapy for bleeding peptic ulcer disease (PUD)
has resulted in the selection of a small subgroup of high-risk
patients for today’s surgeon. It is likely that patients currently
coming to operation for bleeding PUD are at higher risk for a
poor outcome than ever before. The mortality rate for surgery
for bleeding peptic ulcer is around 20%. (See Schwartz 11th
ed., pp. 1131–1133.) Today, most patients undergoing emergent operation have simple patch of a perforated ulcer or oversewing of a bleeding ulcer. (See Schwartz 11th ed., p. 1127.)
Long-term maintenance proton pump inhibitor (PPI) therapy should be considered in all patients admitted to hospital
with ulcer complications, all high-risk patients on NSAIDs or
aspirin (the elderly or debilitated), and all patients requiring
anticoagulation or antiplatelet agents or those with a history of
recurrent ulcer or bleeding. (See Schwartz 11th ed., p. 1125.)
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9. A 50-year-old homeless man is brought to the emergency
room (ER) complaining of 2 days of severe abdominal
pain. He states that he “has had ulcer trouble for 30 years.”
Temp = 102°F, BP = 80/50, P = 130. He has abdominal distention and generalized peritonitis on examination. Serum
lactate is elevated. He is given intravenous (IV) antibiotics
and 2 L of crystalloid then started on norepinephrine drip.
Nasogastric (NG) drains 300 mL of bilious nonbloody
fluid. Computed tomography (CT) scan immediately after
injection of 100 mL oral contrast via NG shows extravasation from the duodenal bulb, copious-free peritoneal fluid,
and air. BP is now 110/70, serum lactate is normal, and
urine output in the past hour is 20 mL. You strongly suspect
perforated duodenal ulcer and you would recommend:
A. Endoscopy and biopsy.
B. Immediate closure of perforation with Graham patch.
C. Nonoperative management.
D. Immediate closure of perforation with definitive
ulcer operation.
E. An additional 8 hours of ICU resuscitation, followed
by laparoscopic patch and highly selective vagotomy.
10. Which of the following options is the least preferable
reconstruction for patients undergoing antrectomy for
peptic ulcer disease?
A. Bilroth I.
B. Bilroth II.
C. Roux-en-Y
gastrojejunostomy.
D. All are equally preferable.
Answer: B
Surgery is almost always indicated for ulcer perforation,
although occasionally nonsurgical treatment can be used
in the stable patient without peritonitis in whom radiologic
studies document a sealed perforation. Simple patch closure,
currently the most commonly performed operation for perforated peptic ulcer, is the procedure of choice in patients with
hemodynamic instability and/or exudative peritonitis signifying a perforation >24 hours old. (See Schwartz 11th ed.,
p. 1134.)
Answer: C
Following antrectomy, gastrointestinal (GI) continuity may be
reestablished with a Billroth I gastroduodenostomy (Fig. 26-3)
or a Billroth II loop gastrojejunostomy (Fig. 26-4). Since antrectomy routinely leaves a 60% to 70% gastric remnant, routine
A
CHAPTER 26
Stomach
FIG. 26-3. A and B. Billroth I
gastroduodenostomy. ( Reproduced with
permission from Zinner MJ. Atlas of Gastric
Surgery. New York, NY: Elsevier/Churchill
Livingstone; 1992.)
B
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