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FIGURE 2.17. Proximal gastric vagotomy. (A and B) The key elements of proximal gastric vagotomy are
to divide the gastric branches of the anterior and posterior vagi at the lesser curvature while preserving the nerve of Latarjet and the innervation of the antral pyloric mechanism. Another key feature of
this operation is “skeletonization” of the distal 6–8 cm of the esophagus. (Adapted from Jamieson GG,
Debas HT, eds. Rob & Smith’s Operative Surgery: Surgery of the Upper Gastrointestinal Tract. London:
Chapman & Hall Medical; 1994.)
Truncal Vagotomy and Antrectomy From the acidreducing perspective and that of postoperative recurrence
of ulcer, truncal vagotomy and antrectomy comprise the
superior procedure for duodenal ulcer. It removes both the
vagal (cholinergic) and gastrin drive of acid secretion. The
ulcer recurrence rate is <0.5%.
4
The problem with the operation is that it creates the potential for the side effects of
both vagotomy and gastrectomy. For this reason, it should
be used rarely to treat uncomplicated duodenal ulcer.
(TV), a simpler operation to do, has retained popularity,
particularly in the United States.It has a low operative mortality, and the incidence of ulcer recurrence is 8% to 10%.
Looseness of bowel occurs in some 10% to 15% of patients
after the operation, but 1% develop debilitating diarrhea
postvagotomy.
to 10% of patients.
4
The dumping syndrome is a problem in 5%
4
Selective total vagotomy is the most
appropriate type of vagotomy to be combined with antrectomy because it preserves hepatic, biliary, pancreatic, and
intestinal vagal innervation. It also reduces the incidence of
Relative Merits of Operative Procedures Worldwide,
PGV is the elective operation of choice for duodenal ulcer.
It has the lowest operative mortality rate and is not
associated with the undesirable side effects seen with other
procedures (e.g., dumping syndrome, diarrhea). Unfortunately, patients treated with PGV have a higher recurrence
postoperative diarrhea.
None of these operations are as effective as vagotomy
and antrectomy (V & A) in preventing ulcer recurrence.
Unfortunately, the low ulcer recurrence rate of <0.5%
comes at the expense of long-term complications from
both vagotomy and gastrectomy.
rate (5% to 20%); now that elective surgery for duodenal
ulcer is rare, few surgeons are appropriately trained to
perform PGV.
C linical M anagement .......................................................................................................................... 59
5
Hence, truncal vagotomy and drainage
LECTIVE SURGICAL PROCEDURES FOR GASTRIC ULCER
E
While vagotomy is the cornerstone of elective surgery for
4
FIGURE 2.18. Types of gastric ulcer. Type I gastric ulcer, one of the most common varieties, occurs in
the antrum of the stomach. In Type II gastric ulcer, the ulcer in the antrum is associated with an ulcer
in the duodenum. Type III gastric ulcer is a prepyloric ulcer.
duodenal ulcer, gastric resection is often more appropriate
to treat patients with gastric ulcer.Two reasons support this
philosophy. First, unlike duodenal ulcer, where increased or
inappropriate acid secretion is invariably a factor, gastric
ulcer appears to be associated more with reduced mucosal
defense. Second, although a duodenal ulcer is nearly always
benign, a gastric ulcer can be malignant. Resection provides
the best chance for the diagnosis and cure of gastric ulcer.
Types of Gastric Ulcer Three types of gastric ulcer have
been described; they are designated as Type I, Type II, and
Type III (Figure 2.18).
1. Type I, the most common type of gastric ulcer, occurs
at the lesser curvature and is typically found in the
transitional mucosa between the body of the stomach
and the antrum.
2. Type II is a gastric ulcer that coexists with a duodenal
ulcer.
3. Type III is a prepyloric or pyloric channel ulcer that
seems to be associated with gastric acid hypersecretion.
Choice of Operation The operation of choice differs
for these three types of gastric ulcer. The best surgical procedure for Type I ulcer is conservative distal gastrectomy,
which can often be limited to antrectomy. A gastroduodenal anastomosis is associated with fewer long-term
complications, and so is preferred over a gastrojejunal
anastomosis.
Patients with Type II gastric ulcers are also best treated
with conservative distal gastrectomy and gastroduodenal
anastomosis. Some surgeons add truncal vagotomy to this
procedure because gastric acid hypersecretion is frequently seen with this type of ulcer. Any benefits of truncal
vagotomy may be outweighed by the long-term sequelae
of postvagotomy diarrhea. A large clinical experience is
now documented to indicate that PGV as the only operation is inappropriate in this setting because ulcer recurrence in patients approaches 40%.
4
Patients with Type III gastric ulcers are more defini-
tively treated with vagotomy and antrectomy. Ideally, a
selective gastric vagotomy should be done to preserve
extragastric vagal innervation and minimize the incidence
of postvagotomy diarrhea.
Management of Complicated Peptic Ulcer
M
ANAGEMENT OF
PERFORATED
PEPTIC ULCER
Perforation still occurs commonly and continues to be a lethal
complication of peptic ulcer disease, particularly in elderly
patients or when treatment is delayed. Its incidence in
elderly patients is rising because of increased use of
NSAIDs. Perforated duodenal ulcer is ten times more
common than perforated gastric ulcer. The essentials of
management are summarized in Table 2.9.
In all abdominal crises, as in multiple trauma, it is
helpful to use a consistent approach that includes resuscitation, diagnosis, and treatment.
Resuscitation: Initial and Secondary Assessments The
patient is in obvious pain and is anxious. Very quickly, the
TABLE 2.9. Essentials: Management of Perforated Peptic Ulcer
Trends
Overall incidence unchanged
Rising incidence in elderly patients
Mortality rate of 10%
Diagnosis
Usually presents with acute abdomen
If accompanied by hypotension, suspect other diagnoses
(ruptured AAA, pancreatitis, mesenteric vascular accident)
If accompanied by blood in nasogastric aspirate, consider
“kissing ulcer”
Only 75%–80% show pneumoperitoneum
Operative technique
Duodenal ulcer: Closure of perforation alone or with
addition of PGV
Gastric ulcer: Distal gastrectomy to include ulcer or local
excision of ulcer
Late perforation: Conservative management if
䊏
Ulcer is sealed
䊏
Peritonitis is absent
Abbreviations: AAA, abdominal aortic aneurysm; PGV, proximal gastric
vagotomy.
60 ..................................................................................................................... Stomach and Duodenum
airway and vital signs are assessed. The breathing is shallow
and rapid as diaphragmatic movement is restricted, but
airway is not usually a problem. A mild tachycardia is
present, but during the early phases of perforation,
hypotension should not be present. If hypotension is
present, other diagnoses should be suspected. These
include ruptured abdominal aortic aneurysm, severe acute
pancreatitis, and mesenteric vascular accident. The initial
survey also reveals the presence of an acute abdomen or
peritonitis with board-like abdominal rigidity, tenderness
and rebound tenderness, and hypoactive or absent bowel
sounds. The patient lies perfectly still, often in the fetal
position.
Once the initial examination is completed (it should
take no more than 1 or 2 minutes), resuscitation is started
with institution of intravenous fluid administration and
insertion of a nasogastric tube to decompress the stomach
and prevent aspiration.
Secondary assessment should include obtaining a full
history and performing a thorough physical examination.
A history of previously diagnosed peptic ulcer or peptic
ulcer–type symptoms may or may not be present. Florid
presentation of an acute abdomen may be absent in a
number of patients with special circumstances. These
include:
1. the very old or very young patient;
2. any patient who is receiving high-dose steroid
therapy, which blunts the peritoneal response;
3. the paraplegic patient, in whom the only symptom
may be tip of shoulder pain;
4. the comatose patient, in whom systemic manifesta-
tion of sepsis is often the first clue; and
5. the patient recovering from an abdominal operation,
where the diagnosis is often delayed as signs and symptoms are assigned to causes related to the recent operation.
Thus, the surgical ward may be the worst place for a
patient to have a perforated ulcer.
Diagnosis A patient’s diagnosis is often established
with his or her medical history and the classic findings
from the physical examination. The patient may have a
slight leukocytosis with some shift to the left and a normal
urinalysis, which often suffice in the typical case. Often,
however, plain abdominal views (supine, upright, and right
decubitus) and a chest x-ray are also obtained. Free gas in
the peritoneal cavity is seen in about 75% of patients
(Figure 2.19). When perforation is suspected but no free
air is seen in the peritoneal cavity, a Gastrografin swallow
may be useful. Endoscopy, however, should be avoided.
When the presentation is not as clear-cut as described
above, other conditions must be included in the differential diagnosis, particularly acute pancreatitis, acute cholecystitis, acute appendicitis, and even acute myocardial
infarction. If the serum amylase level is elevated because of
a perforated peptic ulcer, the elevation is usually lower than
three times the normal level. Leukocytosis tends to be
greater in acute pancreatitis. An abdominal ultrasound,
FIGURE 2.19. Perforated peptic ulcer. This condition may be evident from the history and demonstration of classic findings in physical examination. This patient’s chest x-ray shows air between the right
hemidiaphragm (arrow) and the liver (L) and between the left hemidiaphragm (arrow) and the
stomach (S). (Courtesy of Henry I. Goldberg, MD.)
C linical M anagement .......................................................................................................................... 61
when indicated, is useful in ruling out acute cholecystitis.
An electrocardiogram and serum enzymes may be
necessary to exclude the diagnosis of acute myocardial
infarction.
Once it is decided that an operation will be performed,
analgesia and perioperative broad-spectrum antibiotics
should be administered.
Surgical Management Operative closure of the perforation is the definitive treatment. This operation can be
done laparoscopically or through a limited epigastric
incision, depending on the surgeon’s experience. A classic
approach to closing a perforated duodenal ulcer is the
Graham patch technique (Figure 2.20). Alternatively, the
ulcer can be closed primarily and an omental patch applied
over the suture line.
A secondary approach is to perform an additional
ulcer-reducing procedure. Several prospective randomized
clinical trials
6
have documented that the addition of
proximal gastric vagotomy (see Figure 2.17) to closure of
perforation does not increase the mortality or morbidity
of surgical therapy, but reduces postoperative ulcer recurrence from 40% to 50% to approximately 8%. The following conditions must be confirmed before PGV is added
to the closure procedure.
1. The perforation must be less than 24 hours old;
2. The patient must be hemodynamically stable and free
of any serious cardiac, pulmonary, or renal disease;
3. There must be evidence of ulcer chronicity in either the
history or the operative findings of scarring and distortion of the duodenal bulb.
FIGURE 2.20. Graham patch technique. (A and B) This technique provides a safe and established
method of closure of perforated duodenal ulcer. The ulcer is closed by sutures applied over a piece of
omentum. (Adapted from Schwartz SI, Ellis H, Husser WC, eds. Maingot R. Maingot’s Abdominal
Operations. Stamford, CT: Appleton & Lange, 1989.)
62 ..................................................................................................................... Stomach and Duodenum
C linical M anagement .......................................................................................................................... 63
It must be mentioned, however, that the studies demonstrating the usefulness of PGV were done before the recognition of H. pylori as a cause of ulcer and the development
of effective eradication therapy to prevent recurrence.
Prospective randomized studies are needed to determine
whether PGV is necessary in the era of H. pylori eradica-
tion. The author’s view is that performing truncal vagotomy and pyloroplasty when closing the perforation is not
an optimal acid-reducing procedure because of the potential for troublesome long-term side effects.
Delayed Perforation A patient with a perforation of 48
hours duration or longer may be treated conservatively
with nasogastric suction, intravenous antibiotics, and
parenteral nutrition, as long as peritonitis is absent and
Gastrografin swallow shows that the perforation is sealed.
If a conservative management approach is decided upon,
careful follow-up is necessary to detect early development
of any abdominal abscess. If an abdominal abscess does
develop, diagnosis and treatment by percutaneous catheter
can be accomplished with the aid of an abdominal CT scan.
Nonsurgical Management of Perforation From time to
time, published clinical studies claim that nonsurgical
management is effective. When carefully scrutinized,
however, these studies show flaws that make it difficult to
accept their recommendations. For example, at the University of Southern California, the Gastrografin swallow
test has been used to determine whether the perforation is
sealed or not. If the perforation is sealed and peritonitis is
not present, conservative management of these selected
patients has been used successfully. While this approach
may be necessary when operating room capacity is in short
supply, it is not recommended for general use.
“Kissing Ulcer” Problem Infrequently, a patient who
presents with a perforated duodenal ulcer is found to have
blood in the stomach when nasogastric suction is performed. In these circumstances, the old adage applies:
“Anterior ulcers perforate and posterior ones bleed.” A
patient with unequivocal findings of a perforated duodenal ulcer and concomitant bloody nasogastric aspirate
must be suspected of having a “kissing ulcer,” that is, a perforated anterior ulcer and a bleeding posterior ulcer. At
the time of operation, the posterior wall of the first part of
the duodenum must be examined by extending the hole
from the perforation. In the presence of a bleeding duodenal ulcer, suture control of the bleeding must be accomplished. A definitive ulcer operation is also required. The
choices are to close the perforation and duodenotomy with
an omental patch and perform proximal gastric vagotomy;
or to extend the duodenotomy incision across the pylorus
into the stomach, close this with pyloroplasty, and perform
truncal vagotomy.
Perforated Gastric Ulcer The above discussion on perforated duodenal ulcer applies equally well to perforated
gastric ulcer with one difference.
7
Malignancy, which has
an incidence of 15%, must always be ruled out in a perforated gastric ulcer. This can be accomplished by completely
excising the ulcer or, alternatively, by four-quadrant biopsy
if excision cannot be accomplished successfully. Conservative distal gastrectomy encompassing the ulcer is the initial
therapy of choice. If the ulcer is malignant, a more radical
type of gastrectomy will be needed.
H
EMORRHAGE The most common cause of upper
GI hemorrhage is peptic ulcer. Approximately 20% of
patients with peptic ulcer will bleed. It is likely that, with
H. pylori eradication and proton pump inhibitor therapy,
the incidence of bleeding will decrease. To date, however,
no convincing data support this contention.
Not all bleeding from ulcer is acute or massive. Indeed,
some patients present with iron-deficiency anemia from
occult blood loss. When acute hemorrhage occurs, patients
present with hematemesis and/or melena. Infrequently,
massive bleeding from a duodenal ulcer presents as lower
gastrointestinal hemorrhage without hematemesis. If the
bleeding is rapid, the blood issuing rectally may be red
rather than black.
Some 90% of patients admitted with upper GI hemorrhage from an ulcer stop bleeding spontaneously within 8
hours of admission to a hospital. Of the remainder, about
half are successfully treated endoscopically with injection
therapy or with heater-probe or laser coagulation. The
rare patient has such an exsanguinating hemorrhage that
immediate operation and control of bleeding is necessary
before volume resuscitation can be adequately accomplished. The management is summarized in Table 2.10.
TABLE 2.10. Essentials: Management of Peptic
Ulcer Hemorrhage
General
Bleeding duodenal ulcer: 10 times more common than
bleeding gastric ulcer
90% of patients stop bleeding within 8 h of admission
Endoscopic stigmata of possible further bleeding
Arterial spurting
Visible vessel
Adherent fresh clot at ulcer base
Indications for surgery
Exsanguinating hemorrhage
Failure of control with endoscopically administered therapy
Rebleeding after initial cessation
Choice of operations
Duodenal ulcer
䊏
Suture control of bleeding and vagotomy and pyloroplasty,
or
䊏
Duodenotomy, suture control, and proximal gastric
vagotomy
Gastric ulcer
䊏
Distal gastrectomy including the ulcer
Resuscitation Initial resuscitation should be accomplished quickly. If there is any question about the patient’s
level of consciousness, the airway must be protected with
endotracheal intubation. In most circumstances, such
drastic action is unnecessary. In the initial survey, the
patient should also be carefully examined for any stigmata
of chronic liver disease and oral mucosal hemangiomas.
Quickly, two large-bore intravenous catheters should
be inserted, as well as a nasogastric tube and a Foley
catheter. A blood sample is obtained for complete blood
count (CBC), blood urea nitrogen (BUN), electrolyte
levels, and for a crossmatch of 4 to 6 units. The speed and
type of fluid resuscitation depends on the hemodynamic
status of the patient. Most patients are moderately
hypotensive, and the initial resuscitation can be successfully accomplished with crystalloids (saline or lactated
Ringer’s solution).When hypotension is extreme, however,
immediate blood transfusion should be given, using either
group specific, Rh-negative, or O-negative blood. Some
severely hypotensive patients can be successfully resuscitated quickly with colloids (plasma, albumin, or Hespan)
until fully crossmatched blood is available. When the
patient is hemodynamically compromised, central venous
pressure monitoring, or preferably, pulmonary artery
pressure monitoring is necessary. The goal of resuscitation
is to rapidly restore circulating volume and adequate urine
output (>50 mL/h) and to establish monitoring of vital
signs, urine output, and central venous or pulmonary
arterial wedge pressure measurements.
Aspiration should be prevented by insertion of either
a large nasogastric tube or an Ewald tube. The stomach is
evacuated and lavaged with water or saline. When large
amounts of blood are transfused, it is necessary to monitor
coagulation factors (e.g., platelets, prothrombin time), and
vitamin K administration may be necessary.
Diagnosis Early detection of the source of bleeding is
a key step in management. The best way to identify the
source is with upper GI endoscopy. The ideal time to
perform this examination is (1) when the patient is hemodynamically stable, and (2) when the nasogastric aspirate
following irrigation is pink. Endoscopy identifies the site of
bleeding in about 90% of patients with upper GI bleeding.
The esophagus is easily ruled out as the site of bleeding.
Lesions in the stomach may be obscured by blood clot,
but even then, with persistence and expertise, the entire
stomach can be examined satisfactorily. Bleeding from
duodenal ulcer may be evidenced by the presence of (1)
active bleeding from a posterior ulcer crater; (2) a visible
bleeding vessel; (3) a visible nonbleeding vessel with clot;
or (4) an adherent fresh clot at ulcer base. In 2 and 3, the
visible vessel is the gastroduodenal artery or one of its
major branches (Figure 2.21).
Angiography has a role, but not a frequent one, in the
early detection of the site of hemorrhage. Bleeding has to
occur at the rate of 2 mL/min or more for the test
to succeed. It is most useful when endoscopy has failed to
FIGURE 2.21. Endoscopic view of a visible vessel at the base of
an active ulcer. (Courtesy of John P. Cello, MD.)
identify the cause of bleeding. On occasion, when bleeding is massive and a nonsurgical treatment approach is
chosen, angiography can be useful not only in identifying
the bleeding vessel but also in controlling bleeding by
selective embolization.
Control of Bleeding As indicated earlier, 90% of
patients stop bleeding spontaneously within 8 hours of
admission to a hospital and can be managed conservatively.
If bleeding persists, control with the aid of endoscopy can
be achieved with coagulation (e.g., heater probe, laser),
endoscopic sclerotherapy, or by endoscopic injection of
alcohol or adrenaline.
Surgical Indications The following indications for
surgery for the patient with a bleeding ulcer are generally
accepted:
1. Exsanguinating hemorrhage when quick resuscita-
tion is difficult.
2. Failure of control of hemorrhage with endoscopic-
based methods.
3. Rebleeding that begins again while the patient is
under treatment in a hospital after initial cessation. (This
circumstance nearly always suggests bleeding from a gastroduodenal artery.) Even here, it is reasonable to attempt
endoscopic control before surgery if the patient is stable
and/or at high risk for surgery.
4. Loss of 6 units of blood or more where endoscopic
therapy is unavailable or cannot be performed.
64 ..................................................................................................................... Stomach and Duodenum
The principles of surgery in a bleeding peptic ulcer are
to control bleeding and perform a definitive ulcer
operation. Preferred options are available when the site of
bleeding can be identified as either a duodenal or a gastric
ulcer. When the site of bleeding is uncertain, a distal gastrotomy is first performed so that it can be extended into
the duodenum if necessary.
Surgery for Bleeding Duodenal Ulcer If a duodenal
ulcer is identified as the cause of bleeding, the two surgical
options are (1) truncal vagotomy, pyloroplasty, and suture
control of bleeding or (2) duodenotomy, suture control of
bleeding, and PGV. In the elderly or unstable patient, the
first option is more appropriate; the author prefers the
second option in the young and stable patient.
The technique of controlling a bleeding duodenal ulcer
with sutures is illustrated in Figure 2.22. Nonabsorbable
00 sutures on a stout needle are used. Interrupted sutures
are placed at the proximal and distal parts of the ulcer and
tied. This may control all or most of the bleeding. Then a
U-stitch is used, as shown in the figure, to ligate branches
of the gastroduodenal artery. Additional sutures, including figure-8 sutures, may be needed to arrest the bleeding
completely. If these techniques fail to completely control
the bleeding, the gastroduodenal artery must be dissected
outside the duodenum as it branches off the hepatic artery
and ligated in continuity using 0-silk suture.
In severe, chronic duodenal ulcer disease with
advanced scarring and foreshortening of the first part of
the duodenum, the application of sutures to control bleeding from the ulcer bed poses a potential risk to the
common bile duct. If the risk is considered high, it is
prudent to perform choledochotomy and leave a red
rubber catheter in the CBD until after the hemostatic
sutures are tied. At this point, the surgeon can ascertain
whether the catheter is freely movable, indicating that
no ligation of the duct has occurred. The choledochotomy
is then closed over a T-tube.
Surgery for Bleeding Gastric Ulcer Although a bleeding
gastric ulcer can be treated by underrunning the bleeding
point and performing truncal vagotomy and pyloroplasty,
the preferred surgical approach is to perform a distal gastrectomy that removes the ulcer. When the ulcer is higher
up on the lesser curvature of the stomach, a sleeve resection of the lesser curvature may be performed, encompassing the ulcer. When the ulcer is very high and near the
gastroesophageal junction, the Madlener procedure may be
used. This procedure, which has been successfully utilized
in the past, involves underrunning with sutures to control
bleeding, a four-quadrant biopsy to rule out carcinoma,
and a distal gastrectomy to treat the ulcer diathesis. If the
surgeon can ascertain intraoperatively that the ulcer is H.
pylori–associated, the gastrectomy may be avoided and
eradication therapy administered postoperatively. At the
present time, because no data are available to support
this theoretical approach, it is not recommended.
ANAGEMENT OF GASTRIC OUTLET OBSTRUCTION
M
Gastric outlet obstruction results from fibrous scarring of
chronic duodenal ulcer disease. Symptoms develop over a
long period of time, occasionally more acutely due to
edema caused by acute exacerbation of ulceration. But,
even in the latter circumstance, preexisting scarring and
stenosis are likely to be confirmed. Gastric outlet obstruction occurs less frequently than the complications of perforation and bleeding. It is likely that its incidence has
decreased because of the advent of potent acid-reducing
drugs and identification and eradication of H. pylori.
Essentials of the management are listed in Table 2.11.
Clinical Presentation The symptoms of gastric outlet
obstruction are usually insidious and accompanied by a
chronic history of duodenal ulcer. The initial symptoms are
early satiety, bloating, and halitosis. When vomiting eventually develops, it is usually after the last meal of the day.
The vomitus may contain undigested food eaten 24 to 48
hours earlier. As the obstruction becomes more complete,
vomiting may occur after any meal. Chronic weight loss,
even emaciation, and chronic fatigue develop.
Physical examination may show the presence of “succussion splash” (i.e., a splashing sound in the epigastrium
when the patient is shaken from side to side). Infrequently,
particularly in the emaciated patient, gastric peristalsis
may be visible in the epigastrium.
Investigation A barium meal confirms gastric outlet
obstruction by showing a dilated stomach and a small
amount of barium entering the duodenum (Figure 2.23).
The use of upper GI endoscopy is necessary to exclude
into the duodenum, and no gastric pathology may be
FIGURE 2.22. Suture control of bleeding ulcer requires the
ligature of several branches of the gastroduodenal artery in
the base of the ulcer. One technique uses the U-shaped suture
as shown in the diagram.
C linical M anagement .......................................................................................................................... 65
found. Antral biopsy for histology and H. pylori studies
should be obtained.
The typical biochemical findings when prolonged
vomiting is present are of hypochloremic, hypokalemic,
TABLE 2.11. Essentials: Management of Gastric
Outlet Obstruction
Symptoms and signs
Insidious clinical presentation
Early satiety antedating vomiting
Weight loss
Fatigue
Biochemical goals of treatment
Correction of hypovolemia and hypochloremic, hypokalemic,
metabolic alkalosis
Diagnostic tests
Barium meal
Endoscopy
Conservative therapy (8–10 days)
Continuous gastric decompression
Suppression of acid secretion
Nutritional support with parenteral or enteral nutrition
(percutaneous feeding jejunostomy)
Correction of anemia and vitamin K deficiency
Operative therapy
Assess for “difficult” duodenum
䊏
If present, perform truncal vagotomy and
gastrojejunostomy
䊏
If absent, perform truncal vagotomy and pyloroplasty
Ancillary procedures
䊏
Feeding jejunostomy
䊏
Tube gastrostomy
and metabolic alkalosis. Vomiting results in loss of fluid,
chlorides, and H
kidneys attempt to compensate by retaining Na
+
. Severe dehydration develops, and the
+
.To
accomplish this, potassium is initially exchanged, but as
dehydration progresses and potassium stores become
depleted, H
+
is exchanged for Na+in the renal tubules.
Early in the evolution of biochemical derangements
caused by gastric outlet obstruction, the urine is alkaline;
however, paradoxic aciduria soon develops as H
+
is lost
in the urine, even as systemic metabolic alkalosis is
developing. An electrocardiogram may show the typical
peaked T-waves of hypokalemia.
Starvation leads to hypoproteinemia and potential
vitamin K deficiency. Therefore, nutritional status and
coagulation factors need to be assessed.
Moderate electrolyte disturbances can be corrected
through administration of saline and potassium chloride.
When large amounts of potassium chloride must be
administered rapidly, cardiac monitoring may be necessary. Very rarely, if the metabolic alkalosis is severe (blood
pH > 7.6), either 0.01 N HCl or ammonium chloride
solution may need to be given intravenously.
As blood volume is restored, significant hypoalbuminemia and even anemia may become evident. Early
institution of parenteral or enteral nutrition is essential.
The placement of an enteral catheter through the mouth
is not likely to succeed. If enteral therapy is preferred, a
feeding jejunostomy must be placed either percutaneously
or laparoscopically. In addition, chronic obstruction is
likely to be accompanied by vitamin K deficiency, which
must be corrected.
Nonsurgical Management If a patient’s gastric outlet
obstruction is the result of edema from exacerbation of
duodenal ulcer, conservative management as outlined
above may relieve the obstruction in 8 to 10 days. During
this time, it is necessary to maintain nasogastric suction
and administer acid-reducing therapy and nutritional
support. Any improvement in gastric emptying is assessed
by the volume of gastric aspirate and by the use of the saline
load test (Hunt’s test). If obstruction does not resolve completely within 10 days, it is highly probable that surgical
intervention will be necessary.
Treatment The patient should be treated with nasogastric suction to prevent aspiration. Decompression of the
stomach should also be started to restore gastric muscle
tone. Acid secretion can be suppressed by parenteral
administration of H
-receptor antagonists or proton-pump
2
blockers. This is an important step that helps to rapidly
correct metabolic alkalosis.
The extracellular space volume is severely contracted
and must be replenished by administration of normal
saline (not lactated Ringer’s,which contains fewer chloride
ions). A Foley catheter and central venous pressure
monitor may also be necessary.
FIGURE 2.23. Gastric outlet obstruction. This condition can be
confirmed by a barium meal, which demonstrates a dilated
stomach, an abrupt narrowing of the gastric antrum (arrows),
and scarce barium entering the duodenum. This is an example
of late gastric cancer. (Courtesy of Henry I. Goldberg, MD.)
66 ..................................................................................................................... Stomach and Duodenum
C linical M anagement .......................................................................................................................... 67
Operative Management The following three considerations are paramount in the timing of surgery for gastric
outlet obstruction:
1. Correction of fluid and electrolyte imbalance and
anemia;
2. Improvement of nutritional status by hyperalimentation for 7 to 10 days monitored by measurement of
serum albumin, ferritin, and so on;
3. Improvement of gastric tone by continuous nasogastric suction for 7 to 10 days in the totally atonic
stomach. The clinical impression is that restoration of
gastric tone preoperatively lessens the incidence of prolonged failure of gastric emptying following surgery.
The critical intraoperative step is to examine the duodenum for evidence of any inflammatory mass (often indicating localized perforation) or advanced scarring that
would make closure of the duodenum unsafe. If inflammation or excessive scarring is present, the pyloroduode-
TABLE 2.12. Pathophysiologic Basis of Long-Term
Complications of Ulcer Surgery
Complication Pathophysiologic basis
Recurrent ulcer Incomplete vagotomy
Inadequate gastric resection
Zollinger-Ellison syndrome
Retained antrum syndrome
Postvagotomy diarrhea Unknown
Dumping syndrome Rapid gastric emptying
Fluid shift into intestine, causing
hypovolemia
Release of vasoactive peptides and
amines (VIP, neurotensin,
bradykinin, 5-HT)
Reactive hypoglycemia Excessive release of insulinotropic
peptides from the gut (GLI, GIP)
Secondary hyperinsulinemia
Gastroparesis Unknown
Bile gastritis Duodeno-jejuno-gastric bile reflux
Bile-induced mucosal injury
Iron-deficiency anemia Decreased absorption of dietary iron
Chronic occult blood loss
Megaloblastic anemia Decreased intrinsic factor secretion
following radical subtotal or total
gastrectomy
Malabsorption Steatorrhea
Rapid intestinal transit
Blind-loop syndrome
Osteoporosis Calcium malabsorption
Postgastrectomy Hypochlorhydria or achlorhydria
carcinoma
Abbreviations: 5-HT, 5-hydroxytryptamine; GIP, gastric inhibitory peptide;
GLI, glucagon-like immunoactivity; VIP, vasoactive intestinal peptide.
TABLE 2.13. Essentials: Recurrent Ulcer Following
Surgical Therapy
Causes
Incomplete vagotomy
Inadequate gastric resection
Gastrinoma
Uncommon following distal gastrectomy for gastric ulcer
Diagnosis
Best established by endoscopy
Assess for H. pylori infection and initiate eradication therapy
if present
Evaluate for completeness of vagotomy
Surgical treatment
Necessary if medical treatment fails
Choice of procedure depends on type of initial operation:
䊏
Antrectomy if PGV was initially performed
䊏
Re-vagotomy with or without antrectomy if truncal
vagotomy was initially performed
䊏
Re-vagotomy with or without re-resection if V & A was
initially performed
Abbreviations: PGV, proximal gastric vagotomy; V & A, vagotomy and
antrectomy.
num should be left undisturbed, and truncal vagotomy
and gastrojejunostomy should be performed. If, on the
other hand, pyloroplasty can be performed safely, then
truncal vagotomy and pyloroplasty are the treatment of
choice. In either case, a feeding jejunostomy and tube
gastrostomy should be constructed in anticipation of a
protracted recovery period to restore adequate gastric
emptying. Some surgeons believe that vagotomy and
antrectomy (V & A) is a superior option, but there are
no good data to support the contention.
Long-Term Sequelae of Ulcer Surgery
With the exception of proximal gastric vagotomy (PGV),
any ulcer surgery may be associated with undesirable
long-term sequelae. These and their pathophysiologic
bases are summarized in Table 2.12. The operation least
likely to cause undesirable side effects, PGV, is associated
with the highest incidence of ulcer recurrence. On the
other hand, the operation most likely to cure the ulcer
problem, V & A, can lead to long-term complications.
U
LCER RECURRENCE The causes of ulcer recurrence
are incompleteness of vagotomy, inadequacy of gastric
resection, or both. Occasionally, however, ulcer recurrence
is due to an undiagnosed gastrinoma. Recurrence following distal gastrectomy for gastric ulcer is uncommon. The
incidence of recurrent ulcer after surgery for duodenal
ulcer is higher than other rates of recurrence and depends
on the type of operative procedure used to treat the
primary ulcer (Table 2.13). Following PGV and truncal
vagotomy and pyloroplasty (V & P), the site of ulcer recurrence is usually the duodenum, although it may also be the
stomach. Following truncal vagotomy and gastrojejunostomy (V & GJ), ulcer recurrence is nearly always in the
68 ..................................................................................................................... Stomach and Duodenum
jejunum, next to the stoma; hence, the names stomal and
marginal ulcers.
The evaluation of ulcer recurrence includes endoscopy,
measurement of plasma gastrin levels, assessment of completeness of vagotomy, and tests for presence of H. pylori.
Diagnosis with Upper Gastrointestinal Endoscopy
Barium meal studies are usually not helpful in the diagnosis
of recurrent ulcer. Upper GI endoscopy is the only reliable
method of diagnosis.
Diagnosis with Plasma Gastrin Levels Following all
types of vagotomy not associated with antral resection,
both basal and postprandial hypergastrinemia develop.
Thus, elevated plasma gastrin levels following vagotomy
must be interpreted with caution. If there is concern that
a gastrinoma may be present, a “secretin test” should be
performed to detect a paradoxical rise in plasma gastrin
level following intravenous injection of secretin. If hypergastrinemia is demonstrated in a patient who has had
antrectomy, either a gastrinoma or retained antrum syndrome is present. The latter syndrome develops after
Bilroth II gastrectomy, when antral tissue is left in continuity with the duodenum. Chronic exposure of this tissue
to alkaline secretion leads to G-cell hyperplasia and hypergastrinemia. Again, the secretin test is needed to rule out
the diagnosis of gastrinoma.
Assessment of Completeness of Vagotomy Although a
high basal acid output (>5 mEq/h) is suggestive of an
incomplete vagotomy, the sham feeding (“chew and spit”)
test is more definitive.It evaluates the cephalic phase of acid
secretion.
Diagnosis with Helicobacter pylori Testing Evaluation
for the presence of H. pylori may be accomplished with
endoscopic biopsy, breath test, or serology. If H. pylori
infection is present, eradication therapy is needed.
Treatment If infection with the bacterium H. pylori is
diagnosed, eradication therapy should be started with the
objective of effecting a permanent cure for the ulcer. Combination therapy with amoxicillin or with tetracycline,
metronidazole and omeprazole is effective.
A histamine H
2
-receptor antagonist or proton-pump
inhibitor provides symptomatic relief but is unlikely to
cure the recurrence of the ulcer.
The type of operation needed if medical therapy fails
depends on the primary operation that was performed
(see Table 2.13).
P
OSTVAGOTOMY
DIARRHEA
The incidence of incapac-
itating diarrhea following truncal vagotomy is 1% to 2%.
8
The cause is unknown. Symptomatic treatment includes
avoidance of certain foods and the use of bulk-forming
agents (Kaopectate), codeine, and Lomotil. Postvagotomy
diarrhea has no satisfactory treatment and is best avoided
by performing PGV rather than truncal vagotomy as the
primary procedure of choice. Surgical therapy for postvagotomy diarrhea is a last resort. If pyloroplasty was previously performed, pyloric sphincter reconstruction, which
reverses the pyloroplasty, has had some success. If a gastrojejunostomy was performed, it can be taken down. The
most controversial procedure is the interposition of a 6inch segment of reversed jejunum between the stomach
and duodenum or jejunum to slow intestinal transit. The
reported results are not very encouraging and the procedure is rarely, if ever, recommended. Hence, the best
form of treatment is prevention.
D
UMPING SYNDROME Rapid entry of hyperosmolar
chyme into the intestine as a result of destruction, resection, or bypass of the pyloric sphincter is the main cause of
this side effect. Vagotomy, which interferes with gastric
accommodation, contributes to rapid gastric emptying.
Within 15 to 30 minutes of a meal, the patient experiences
epigastric distress, sweating, flushing, and profound
fatigue. Exaggerated bowel sounds (borborygmi) and
sudden diarrhea may also be experienced. As described
earlier, the underlying cause of the syndrome is the combination of fluid shift into the intestine, which causes
hypovolemia, and the release of vasoactive substances from
the intestine.
R
EACTIVE HYPOGLYCEMIA Patients may develop
typical signs and symptoms of hypoglycemia 90 to 120
minutes after a meal. In extreme cases, hypoglycemic crisis
may develop. This side effect used to be called the “late
dumping syndrome.” The pathophysiologic basis appears
to be rapid absorption of glucose from the intestine, which
leads to excessive secretion of insulin due to release of the
insulinotropic peptide glucagon-like immunoactivity
(GLI), which outlasts the hyperglycemic stimulus. Avoidance of carbohydrates in the diet is helpful. The long-acting
somatostatin analogue octreotide is effective in controlling
severe symptoms.
G
ASTROPARESIS A small percentage of patients may
develop gastroparesis following vagotomy and/or gastric
resection. The cause is unknown. Symptomatic therapy
with prokinetic agents (e.g., dopamine antagonists, cisapride) may be helpful. Some patients require repeated
gastric resections, eventually necessitating total gastrectomy with Roux-en-Y esophagojejunostomy. In some
patients with disabling symptoms, total gastrectomy is the
only definitive and successful treatment.
B
ILE
GASTRITIS
Regurgitation of bile into the stomach
invariably occurs when the pylorus is destroyed, resected,
or bypassed. Some patients develop epigastric pain and
bilious vomiting presumably due to the resultant gastritis.
Medical therapy includes bile salt antagonists and prokinetic agents. Bile reflux can be prevented or minimized
by inserting a 60-cm Roux-en-Y jejunal limb between the
stomach and upper jejunum. Unfortunately, the early
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