COMPLICATIONS OF GASTRIC AND DUODENAL ULCERS
The two most serious complications of gastric or duodenal peptic ulcers are perforation and hemorrhage. The frequency of acute perforations in patients hospitalized for peptic ulcer varies from 2% to 25%. Perforation occurs with far greater frequency in men than in women. It is also recognized that peptic ulcer tends to perforate more often in individuals between the ages of 25 and 50 years than in younger or older persons. Fortunately, these two complications appear to have decreased over the last several decades with the wide-spread use of flexible upper endoscopy for diagnosis of ulcer disease and the advent of improved medical treatments with proton pump inhibitors and for H. pylori infection.
The previous
duration of an ulcer, of either the stomach or the duodenum, seems to have no
influence on the speed with which the ulcerative and inflammatory processes
penetrate the muscular coat and the serous layer. An acute peptic ulcer may
rapidly penetrate or perforate the gastric or intestinal wall, so that, in some
instances, the patient may fail to give any history of typical ulcer symptoms.
Many chronic ulcers, on the other hand, may exist for years without progressing
so far in depth as to implicate the serosa, although no chronic ulcers with
severe and persistent symptoms or recurrent or calloused ulcers are ever exempt
from the potential danger of a perforation. The rapidity with which the
digestive effect of the strongly acid gastric juice destroys the layers of the
wall and approaches the serosa cannot be anticipated.
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Once
perforation has taken place, the location of the ulcer plays an important role
as to the clinical presentation of the patient. Ulcers of the anterior wall of
both the stomach and the duodenum have a greater access to the “free”
peritoneal cavity than do those on the posterior wall. From the posterior
aspects, the ulcer may proceed to penetrate the underlying organs such as the
left lobe of the liver, the pancreas, or the gastrohepatic ligament. These may
block the ulcer and prevent the entry of gastric or duodenal contents into the
peritoneal cavity. This “walled-off” perforation, in which a new floor for the
ulcer has been organized outside the visceral wall, has been called chronic
perforation or penetration; the term subacute perforation has
been reserved for certain tiny ruptures in the serosa, which occur only with a
relatively slowly advancing penetration of a chronic gastric ulcer. In such
instances, fibrinous adhesions to contiguous parenchymal organs or peritoneal
attachments have come into existence, as a result of periinflammatory tissue
reactions, long before the ulcer has penetrated to the serosal layer. The
adhesions intercept the small amount of gastric content that might escape
through what are usually very small apertures, thus enveloping the fluid, which
may lead to the development of localized abscesses.
A free
perforation occurs most frequently with ulcers of the anterior wall of the
duodenal bulb. The hole resulting from an acute perforation is usually round,
varying in diameter from 2 to 4 mm. One of the characteristic features of these
holes is their sharp edges, which make them appear to have been punched out. The surrounding tissue
may fail to show any signs of chronic induration, edema, or inflammation.
The clinical
picture of an acute and free perforation, whether it occurs in the stomach or
in the duodenum, is often dramatic. At the moment of perforation, the patient
is seized by a sudden, excruciating, explosive pain, which is of a severity
“almost beyond description.” It is felt all over the abdomen and may radiate to
the chest and shoulder. The patient is pale, the haggard face is covered with cold
perspiration, and the suffering is expressed in every feature of the
countenance. In an effort to reduce the abdominal pain, the patient flexes the
thighs toward the abdomen, which is extremely rigid and tender (“doubling up”).
During this early phase, which may last from 10 minutes to a few hours, in part
depending on the amount and type of gastrointestinal content released into the
peritoneal cavity, the body temperature is subnormal; the pulse and blood
pressure remain within the normal range (or the rate of the pulse may even be
rather slow), though respiration may assume a superficial and panting
character. Within a short time, in some instances introduced by a period of
apparent subjective improvement, all the typical signs (e.g., nausea, vomiting,
dry tongue, rapid pulse, fever, leukocytosis) of a severe, acute, diffuse
peritonitis appear. The tenderness, in the early phase confined mostly to the
upper part of the abdomen, has spread, as a rule, over the total abdominal
area. It may be excessive in the lower right quadrant if, with a perforation of
a duodenal ulcer, the intestinal material is dissipated in the right lumbar
gutter along the ascending colon.
The
differential diagnosis between a perforated gastric or duodenal ulcer and
pancreatitis or a mesenteric thrombosis may be rather difficult in some cases,
but such difficulties are seldom encountered with a ruptured appendix. Other
conditions, such as an ectopic pregnancy, ruptured diverticulum, renal colic,
acute episodes of biliary tract diseases, acute intestinal obstruction or volvulus,
and, in some instances, coronary thrombosis, must also be considered.
The sign
that is most helpful in confirming the suspected diagnosis of ulcer perforation
is the presence of free air in the peritoneal cavity, particularly in
the sub-phrenic space, demonstrable by upright x-ray examination. If it
is possible for the patient to sit or stand, the air will accumulate under the
diaphragm. Escaped air is present, in rare cases, under the left diaphragm
only; not infrequently air may be detected under both diaphragmatic leaves and,
more usually, under the right leaf only.
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Surgical
intervention is nearly always required in the form of exploratory laparotomy
and closure of perforation with peritoneal wash. Conservative treatment,
including intravenous fluids, antibiotics, nasogastric aspiration, and bowel
rest, is occasionally used with consultation with surgery, if the patient is
nontoxic and clinically stable. With the finding of air, operation is usually
indicated without delay. The prognosis of a perforated gastric or duodenal
ulcer is better the earlier an operation is performed. The mortality rate
increases when the operation is performed more than 6 hours after perforation.
The operation of choice is often a subtotal gastric resection in younger individuals
who are in good general condition. This is true if the surgeon is permitted to
work within the first 6 hours after the ulcer has perforated, under optimal
hospital conditions, with carefully supervised anesthesia, with the support
necessary to combat successfully the vascular collapse and infection. When the
patient is in poor general condition, efforts to treat conservatively with
suction through an indwelling catheter in the stomach, massive antibiotics, and
supportive therapy entail a greater risk and are less successful than is
surgical treatment, although in some isolated instances the life of the patient
so treated has been saved. The simple closure of the perforation, postponing
the more definitive surgery, if necessary, until such time as the patient may
be in a more favorable condition, should be reserved for cases that come to the
surgeon’s attention later than 6 hours after the onset of the acute illness, or
for elderly patients (over 60 years of age), when the shock tends to be massive, or when the
cardiopulmonary situation requires an operation of the shortest possible
duration. In approximately 60% of cases in which the perforation is closed by
simple suture, the more radical operation becomes inevitable at a later time.
The symptoms
of a spontaneously closing ulcer perforation (so-called subacute perforation)
lack the dramatic accents of an “acute” or free perforation. The majority of
these patients may not feel more than some intensification of their usual ulcer
pains. It happens, not infrequently,
that a perforation is not detected preoperatively in the assessment of a
bleeding or intractable ulcer but becomes evident only at surgery or with
examination of the pathologic specimen. In other instances the patient, as well
as the physician, may have been well aware of the acute event, but the signs
pointing to a perforation (e.g., sharp epigastric pain, abdominal rigidity,
elevated temperature and pulse rate) disappeared within such a short period of
time that operation was deferred as not critical. Sooner or later, however, most of these patients
must be operated upon because of a localized peritonitis, an abscess that may
form in the subphrenic or subhepatic regions, or, later, a partial gastric or
duodenal obstruction caused by the massive scar formation.
The erosion
of the serosal layer by a chronic peptic ulcer on the posterior walls of the
stomach and duodenum and its penetration into a contiguous organ is such a slow
process that the actual perforation is rarely detected by the patient. The
typical ulcer pains and their relation to and relief as a result of food intake
gradually give way to continuous, gnawing, boring pain, which no longer
responds to the ingestion of food. The pain may radiate to the back, shoulder,
clavicular areas, or umbilicus, or downward to the lumbar vertebrae and the
pubic or inguinal regions. Considering the peripheral distribution of pain
pathways and their origin in a spinal segment, the site where the patient
allocates the radiating pain or the detection of a hyperesthesia in a certain
region of the skin may give a clue to determining the organ involved. A classic
example of a chronic perforation is the ulcer of the posterior wall
of the duodenal bulb, penetrating into and walled off by the pancreas. In
operating for this condition and attempting to remove the entire ulcer with its
floor in the pancreatic tissue, one runs the risk of producing a pancreatic
lesion that may open accessory pancreatic ducts. It is, therefore, advisable in
these cases to leave the ulcer floor untouched after careful dissection of the
ulcer from the duodenal wall.
Ulcers located in the upper
parts of the posterior duodenal wall have a great tendency to penetrate
the hepato-duodenal ligament. This process is usually accompanied by the
development of extensive, fibrous, and thickened adhesions, to which the
greater omentum may contribute. The supraduodenal and retroduodenal portions of
the common bile duct, taking its course within the leaves of the ligament, may
become compromised in these adhesions. As a result of a constriction or
distortion of the common duct, a mild obstructive icterus may confuse the
clinical picture. Fortunately, perforation into the duct, with a subsequent
cholangitis, is a rare event. In the surgical approach to an ulcer of that
kind, the anatomic relations of the common bile duct must be kept acutely in
mind, whether or not signs of duct involvement are present. Disastrous lesions
can be avoided by a preliminary exposure of the duct and by the introduction of
a T tube, which serves as a good guide in disentangling the adhesions and
exposing the duodenal wall and the ulcer. Very seldom does an acute perforated
ulcer of the posterior gastric wall release chyme into the bursa omentalis,
producing only signs of localized peritonitis without free air in the abdominal
cavity.
Another
complication of the chronic relapsing duodenal, pyloric, or prepyloric ulcer is
stenosis of the pylorus, which develops gradually as the result of the
little-by-little thickening of the duodenal wall and the progressive fibrotic
narrowing of the lumen. The incidence of complete pyloric stenosis as a sequel
to an ulcer has decreased in recent decades, apparently because of improved medical
management of this type of ulcer and prompt recognition of its initial phases.
Medical management involves the use of proton pump inhibitor therapy; treatment
of H. pylori infection, if present; and, if needed, endoscopic pyloric
dilation. When the pyloric lumen begins to narrow, the stomach tries to
overcome the impediment by increased peristalsis, and its muscular wall becomes
hypertrophic. This is the stage that has been called compensated pyloric
stenosis because, with these adaptation phenomena, the stomach succeeds in expelling
its contents with only mild degrees of gastric retention. Later, when the lumen
is appreciably narrowed, the expulsive efforts of the stomach fail, and the
clinical picture will be dominated by incessant vomiting and by distress, owing
to a progressive dilatation of the stomach, which, at times, may become
massive. This condition of decompensated pyloric stenosis, which results
in the retention of ingested material and the products of gastric secretion,
is, as a rule, irreversible and is an unequivocal indication for surgical intervention. The
operation of choice is a subtotal gastrectomy, but, in view of the
characteristically poor general condition of the patient, the surgeon may
sometimes have to resort to less radical procedures, such as a
gastrojejunostomy. In the presence of a still-active ulcer, those operations
which reroute the gastric content around the duodenum in the simplest fashion
should be supplemented by a bilateral vagotomy.
Minor
bleeding occurs in the majority of patients with acute or chronic peptic ulcer.
“Occult” blood can be found with fair regularity in the stools or gastric juice
of most ulcer patients. This is the result of the oozing characteristic of
ulcerative lesions. Massive hemorrhage, which, together with perforation,
typifies the most dangerous of all ulcer complications, is fortunately far less
frequent. Reliable figures of its incidence are not available, but it has been
estimated that, of all massive hemorrhages of the gastrointestinal tract, 60%
to 75% stem from a peptic ulcer. Obliterative endarteritis or thrombosis of the
mucosal and submucosal vessels in the ulcerated tissue may be a natural
protection against bleeding from the more superficial ulcers. As a rule, the hemorrhage
is caused by erosion into a large vessel, though excessive bleeding
occasionally also derives from smaller arteries or veins whose drainage is
impaired. A decisive factor for the degree of bleeding is the location of the
ulcer. Gastric ulcers have often caused excessive blood loss, but the most
frequent origin of a massive hemorrhage is the ulcer of the posterior
portion of the duodenal bulb, because here the ulcer can penetrate into the
walls of the gastroduodenal and retroduodenal (posterior and superior
pancreaticoduodenal) arteries, which course just behind the first portion of
the duodenum.
The
essential clinical signs of a duodenal ulcer perforated into an artery are
massive melena and acute vascular collapse. The shock may appear suddenly and
very shortly after the opening of an artery, or it may be delayed for several
hours. In striking contrast to the hemorrhages due to gastric ulcer and
esophageal ulcers or varices, hematemesis is rare with bleeding from a duodenal
ulcer, because the blood, originating from beyond the spastic pylorus, is
propelled into the small intestine and does not regurgitate to the stomach. In
some cases sudden bleeding comes as a complete sur- prise to patients who have
had no previous complaints or signs pointing to the presence of an ulcer, and
this may be the first event to indicate the existence of a “silent” ulcer. The
differential diagnosis of the origin of the bleeding and its localization may,
at times, be extremely difficult. Emergent upper endoscopy in patients with
upper gastrointestinal bleeding is usually indicated. X-ray examination is
often of little help, because such a bleeding ulcer may fail to show the
usually typical perifocal changes, and because the niche may be filled with
blood coagulum. Endoscopic therapy with electrocautery, clipping, or injections
is attempted to stop the bleeding, along with giving intravenous fluids and/or
blood and with proton pump inhibitor therapy.
Massive and
continuous bleeding from an ulcer which cannot be stopped endoscopically should
be treated surgically. Repeated hemorrhages are adequate indication for
surgical intervention. A rapid major blood loss, the advanced age of a patient,
and the presence of shock not immediately responsive to appropriate measures
make operation imperative.
Even during
operation, it may often be difficult to establish the origin of hemorrhage if
it has not been determined before surgery by upper endoscopy.
However,
endoscopic localization can also be difficult if the bleeding is massive. A
bluish discoloration of the upper jejunal loops permits no more than a
suspicion that the bleeding has originated in the gastroduodenal or esophageal
area. The ulcer itself cannot always be palpated, and only after duodenotomy
may the ulcer crater be found. The bleeding can then be provisionally secured
by ligation of the bleeding vessel. The final arrest of the hemorrhage,
however, may require subtotal resection.
