A PEPTIC ULCER is a nonmalignant, mucosal lesion of the stomach or
duodenum in which acid and pepsin play major pathogenic roles. The major forms
of peptic ulcer are duodenal ulcer (DU) and gastric ulcer (GU). Gastric and
duodenal ulcers are breaks in the gastric and duodenal mucosa. Both gastric and
duodenal ulcers relate to the corrosive action of pepsin and hydrochloric acid
on the mucosa of the upper gastrointestinal tract. Ulcers generally range
between 3 mm and several centimeters in diameter.
DIAGNOSING
PEPTIC ULCER
Diagnosis from a
qualified medical practitioner is required. Clinical diagnosis must be supported
by appropriate history and physical examination data. Upper gastrointestinal
(UGI) x-ray or UGI endoscopy is often useful. However, a negative UGI report
does not exclude the existence of an ulcer. The onset of peptic ulcer disease
may be established when classical clinical symptoms manifest. A definitive
diagnosis can be established by gastroscopic examination at a later date. Results
from Helicobacter pylori (H. pylori) breath test and/or serology, if completed, should be
submitted.
Most patients with
peptic ulcer disease present with abdominal discomfort, pain or nausea. The
pain is located in the epigastrium and usually does not radiate. However, these
symptoms are neither sensitive nor specific. Pain radiating to the back may
suggest that an ulcer has penetrated posteriorly, or the pain may be pancreatic
in origin. Pain radiating to the right upper quadrant may suggest disease of
the gallbladder or bile ducts. Patients may describe the pain of peptic ulcer
as burning or gnawing, or as hunger pains slowly building up for 1–2 hours,
then gradually decreasing. Useof antacids may provide temporary relief.
Classically, gastric ulcer pain is aggravated by meals, whereas the painof
duodenal ulcers is relieved by meals. Hence, patients with gastric ulcers tend
to avoid food and present with weight loss, while those with duodenal ulcers do
not lose weight. It is important to remember that although these patterns are
typical, they are not pathognomonic. The nature of the presenting symptoms
alone does notpermit a clear differentiation between benign ulcers and gastric
neoplasm.
ANATOMY
AND PHYSIOLOGY
The stomach is located
in the upper part of the abdomen just beneath the diaphragm. The stomach is
distensible and on a free mesentery, therefore, the size, shape, and position
may vary with posture and content. An empty stomach is roughly the size of an
open hand and when distended with food, can fill much of the upper abdomen and
may descend into the lower abdomen or pelvis on standing. The duodenum extends
from the pylorus to the ligament of Treitz in a sharp curve that almost
completes a circle. It is so named because it is about equal in length to the
breadth of 12 fingers, or about 25 cm. It is largely retroperitoneal and its position
is relatively fixed. The stomach and duodenum are closely related in function,
and in the pathogenesis and manifestation of disease.
The stomach may be
divided into seven major sections. The cardia is a 1–2 cm segment distal to the
esophagogastric junction. The fundus refers to the superior portion of the
stomach that lies above an imaginary horizontal plane that passes through the
esophagogastric junction. The antrum is the smaller distal one-fourth to one-third
of the stomach. The narrow 1–2 cm channel that connects the stomach and
duodenum is the pylorus. The lesser curve refers to the medial shorter border
of the stomach, whereas the opposite surface is the greater curve. The
angularis is along the lesser curve of the stomach where the body and antrum
meet, and is accentuated during peristalsis.
The duodenum extends
from the pylorus to the ligament of Treitz in a circle-like curve and is divided
into four portions. The superior portion is approximately 5 cm in length,
beginning at the pylorus, and passes beneath the liver to the neck of the
gallbladder. The first part of the superior portion (2–3 cm) is the duodenal
bulb. The descending or second part of the duodenum takes a sharp curve and
goes down along the right margin of the head of the pancreas. The common bile
duct and the pancreatic duct enter the medial aspect of this portion of the
duodenum at the major papilla either separately or together. The duodenum turns
medially, becoming the horizontal portion, and passes across the spinal column,
inclining upward for 5–8 cm. The ascending portion begins at the left of the
spinal column, ascending left of the aorta for 2–3 cm, and ends at the ligament
of Treitz, where the intestine angles forward and downward to become the
jejunum.
The normal gastric
mucosa consists of several different secreting cells: endocrine (enterochromaffin-like
[ECL]), gastric, chief, parietal, and mucous neck cells. These cells function
together to secrete gastric juices to aid in the digestive process within the stomach.
The hormone gastrin is secreted by the gastric cells. Gastrin is responsible for
action on the ECL cells, which release histamine, the most important stimulant
of gastric acid secretion. The chief cells secrete pepsinogen, which is
converted to the active enzyme pepsin by hydrochloric acid secreted by the
parietal cells. Mucous neck cells provide a protective barrier for the gastric
lining by secreting mucous. The two types of peptic ulcers discussed are
duodenal and gastric, both located in the upper gastrointestinal tract.
Duodenal ulcers account
for the majority of peptic ulcers. They develop when there is a disruption in
the mucosal defence and the balance between acid-pepsin secretion. In contrast
to those affected by duodenal ulcer, gastric ulcer patients have normal acid secretory
rates. The gastric ulcer is deep, penetrating beyond the mucosa of the stomach,
and histologically similar to duodenal ulceration. Extensive involvement, however,
of the surrounding tissue usually occurs more frequently in gastric than in duodenal
ulcers. The majority of benign gastric ulcers are found immediately distal to the
junction of the antral mucosa. Smokers have a higher incidence of peptic ulcer
disease. Smoking cessation is associated with recovery of gastric function
within hours. Thus, once smoking has ceased, the increased risk of peptic ulcer
disease is removed.
CLINICAL
FEATURES
Some individuals with
active duodenal ulcer have no ulcer symptoms. Thus, there is felt to be an
underestimation of duodenal ulcer frequency. Many signs and symptoms of peptic
ulcer disease are obscure and confusing. Persons may complain only of
indigestion or other vague dyspeptic symptoms commonly found in other
conditions.
Chronic duodenal ulcer
frequently presents with epigastric pain, sometimes situated more to the right
of the epigastrium or central upper abdomen. The pain varies markedly in nature
and intensity from being sharp and burning to aching or gnawing. Characteristically,
the pain occurs from 90 minutes to 3 hours after eating and frequently awakens
the person at night. The pain is usually relieved in a few minutes by food or
antacid. Episodes of pain may persist for periods of several days to weeks or months.
Although symptoms tend to be recurrent and episodic, duodenal ulcers often
recur in the absence of pain. Periods of remission usually last from weeks to years
and are almost always longer than the episodes of pain. In some persons the
disease is more aggressive with frequent and persistent symptoms, or
development of complications. Vomiting of blood may occur.
On physical
examination, epigastric tenderness is the most frequent finding, usually in the
midline and often midway between the umbilicus and the xiphoid process. In
gastric ulcer, epigastric pain is the most common symptom, but the pattern is
less characteristic than with duodenal ulcer. The pain may be precipitated or
aggravated by food, and may or may not respond to antacids. Ulcers may heal and
then recur. Vomiting of blood may occur. While nausea and vomiting almost
always indicate gastric outlet obstruction in duodenal ulcer, these symptoms in
a gastric ulcer may occur in the absence of mechanical obstruction. Gastric
ulcers are associated with weight loss due to anorexia or aversion to food
developing from the discomfort produced by eating. H. pylori infection is associated with 90-95% of duodenal ulcers
and 60-80% of gastric ulcers.
Recognition of the role of H.
pylori in the development of peptic ulcer disease has brought about
substantial changes to the clinical treatment of people with peptic ulcer
disease and has allowed a re-evaluation of the clinical approach to dyspepsia depending
on whether or not a person has H. pylori in
the upper GI tract. H. pylori is
associated with a greatly increased risk of duodenal and gastric ulceration. It
is important to note, however, that while the infection is extremely common
throughout the world and that approximately 50% of adults in developed
countries are colonized by the age of 60 years, not all of these persons will
develop or have had peptic ulcer disease. A number of studies have demonstrated
that it is present in areas of overcrowding or highly infective areas. A
negative UGI x-ray report does not exclude the existence of an ulcer. If
scarring or deformity is present on x-ray or gastroscopic findings, it is
considered that peptic ulcer disease has been present for at least 3 to 4 years.
A positive diagnosis can usually be established when classical symptoms are
described.
CAUSES
AND/OR AGGRAVATION
THE
TIMELINES CITED BELOW ARE NOT BINDING. EACH CASE SHOULD
BE
ADJUDICATED ON THE EVIDENCE PROVIDED AND ITS OWN MERITS.
1. Helicobacter
pylori (H. pylori) prior to onset or aggravation.
H.
pylori is the etiologic factor in most patients with peptic
ulcer disease and may predispose individuals to the development of gastric
carcinoma. H. pylori colonizes in the
human stomach. The method of H. pylori transmission
is unclear, but seems to be person-to-person spread via a fecal-oral route. The
prevalence of H. pylori in adults
appears to be inversely relatedto the socioeconomic status. It is also thought
that water is a reservoir for transmission of H. pylori
2. Ingestion of non-steroidal anti-inflammatory
drugs (NSAIDs) at time of clinical onset or aggravation.
A small but important
percentage of patients have adverse gastrointestinal events associated with
NSAID use that results in substantial morbidity and mortality. Risk factors for
the development of NSAID-associated gastric and duodenal ulcers include
advanced age, history of previous ulcer disease, concomitant use of corticosteroids
and anticoagulants, higher doses of NSAIDs, and serious systemic disorders. The
concept of gastroduodenal mucosal injury has evolved from the notion of topical
injury to concepts that involve multiple mechanisms. NSAIDs initiate mucosal
injury topically by their acidic properties. By diminishing the hydrophobicity of
gastric mucus, endogenous gastric acid and pepsin may injure surface
epithelium. Systemic effects of NSAIDs appear to play a predominant role
through the decreased synthesis of mucosal prostaglandins. The precursor of prostaglandins,
arachidonic acid, is catalyzed by the two cyclo-oxygenase isoenzymes,
cyclo-oxygenase-1 and cyclo-oxygenase-2. The gene for cyclo-oxygenase-1, the
housekeeping enzyme, maintains the homeostasis of organs. Cyclo-oxygenase-2,
the inflammatory enzyme, is inducible. Although NSAIDs can inhibit both pathways,
only the gene for cyclo-oxygenase-2 contains a corticosteroid-responsive
repressor element. Literature suggests that the anti-inflammatory properties of
NSAIDs are mediated through inhibition of cyclo-oxgenase-2, and adverse
effects, such as gastric and duodenal ulceration, occur as a resultof effects on
the constitutively expressed cyclo-oxygenase-1.
For NSAIDs to cause or
aggravate peptic ulcer disease, signs/symptoms of peptic ulcer disease should
develop during the NSAID therapy or within 30 days of cessation of the therapy.
Ingestion of NSAIDs is associated with a higher incidence of peptic ulcer disease.
3. Ingestion of oral corticosteroids at time of
clinical onset or aggravation. For oral
corticosteroids to cause or aggravate peptic ulcer disease, signs/symptoms of
peptic ulcer disease should develop during the corticosteroid therapy or within
30 days of cessation of the therapy.
Minimum dosage levels
and duration of treatment which can cause and/or aggravate ulcers varies among
individuals, and according to their disease and other medications ingested. The
risk of developing peptic ulcer disease while ingesting oral corticosteroids
may be increased even further when NSAIDs are used concurrently.
4. Hepatic cirrhosis prior to clinical onset or
aggravation.
Persons with hepatic
cirrhosis have an increased incidence of peptic ulcer disease.
5. Stress: aggravation only.
Numerous studies have
revealed conflicting conclusions regarding the role of psychological factors in
the pathogenesis and natural history of peptic ulcer disease. The role of
psychological factors is far from established. Acute stress results in
increases in pulse rate, blood pressure and anxiety, but only in those patients
with duodenal ulcers did acute stress actually result insignificant increases
in basal acid secretion. There is no clearly established “ulcer-type”
personality. Ulcer patients typically exhibit the same psychological makeup as
the general population, but they appear to perceive greater degrees of stress.
In addition, there is no evidence that distinct occupational factors influence
the incidence of ulcer disease.
For stress to aggravate
peptic ulcer disease, increased signs/symptoms of peptic ulcer disease should
develop during the period of stress and persist, on a recurrent or continuous
basis, for a period of at least 6 months. There is considerable medical
research available on the impact of prolonged psychologic stress on visceral
function and organic disease. It has not been possible to establish an
association between stress and ulcer formation in controlled studies. Peptic ulcer disease is, however, often
exacerbated, i.e. temporarily worsened, during or shortly after stressful life
events such as occupational, financial and educational problems, divorce or
marital separation, death, and family illness. The role of stress in
aggravation, i.e. permanent worsening, is not settled; any association between
psychologic factors and ulcer disease is likely to be complex and multifactorial.
An individual’s reaction to stress may determine whether a permanent worsening
occurs. Aggravation, or permanent
worsening, may be demonstrated by, but not limited to, the following:
1. Requirement for ulcer-specific medication;
2. Progression in frequency of use of
ulcer-specific medication;
3. Requirement for surgery for peptic ulcer
disease;
4. Development of complications, e.g. bleeding,
outlet obstruction, dumping
syndrome.
6. Zollinger-Ellison Syndrome.
Zollinger-Ellison
syndrome (gastronomas) can produce peptic ulcer disease through hypersecretion
of gastric acid within the upper gastrointestinal tract, thereby disturbing the
delicate acid-pepsin balance. If peptic
ulcer disease is caused by Zollinger-Ellison syndrome, entitlement should be
sought for Zollinger-Ellison syndrome.
7. Inability to obtain appropriate clinical
management
8.
Smoking
The literature reveals
a strong positive correlation between cigarette smoking and the incidence of
ulcer disease, mortality, complications, recurrences and delay in healing
rates. Smokers are about two times more likely to develop ulcer disease than
nonsmokers. Cigarette smoking and H.
pylori are co-factors for the formation of peptic ulcer disease. There is a
strong association between H. pylori infection
and cigarette smoking in patients with and without peptic ulcers. Cigarette
smoking may increase susceptibility, diminish the gastric mucosal defensive
factors, or may provide a more favorable milieu for H. pylori infection.
9.
Alcohol and Diet
Although alcohol has
been shown to induce damage tothe gastric mucosa in animals, it seems to be
related to the absolute ethanol administered (200 proof). Pure ethanol is lipid
soluble and results in frank, acute mucosal damage. Because most humans do not
drink absolute ethanol, it is unlikely there is mucosal injury at ethanol
concentrations of less than 10% (20 proof).Ethanol at low concentrations (5%)
may modestly stimulate gastric acid secretions; higher concentrations diminish acid
secretion. Though physiologically interesting, this has no direct link to ulcerogenesis
or therapy. Some types of food and beverages are reported to cause dyspepsia.
There is no convincing evidence that indicates any specific diet causes ulcer
disease. Epidemiologic studies have failed to reveal a correlation between
caffeinated, decaffeinated, or cola-type beverages, beer, or milk with an
increased risk of ulcer disease. Dietary alteration, other than avoidance of
pain-causing foods, is unnecessary in ulcer patients.
COMMON
MEDICAL CONDITIONS WHICH MAY RESULT IN WHOLE OR IN PART FROM PEPTIC ULCER
DISEASE AND/OR ITS TREATMENT
Intestinal obstructions secondary to
adhesions
Hiatus hernia
Antrectomy and/or
partial gastrectomy are surgical procedures for duodenal ulcer. In the course
of these procedures the esophageal hiatus has to be dissected free in order to
expose the vagus nerves. The interference with the esophageal hiatus may
contribute to the development of hiatus hernia. Vagotomy, if involving
esophageal dissection, may also contribute to the development of hiatal hernia.
The time interval following surgery and the development of the hernia, and age,
are factors in consideration of the degree of consequentiality. No specific
recommendations in respect of the time interval can be made, but the hiatal
hernia would generally occur within a few months of the surgery. There is an
increased incidence of hiatus hernia with age.
Gastroesophageal reflux disease
Interference with the
esophageal hiatus during surgical procedures such as vagotomy may predispose to
reflux esophagitis. The time interval between an operation and the development
of esophageal reflux is a consideration in the degree of consequentiality. No
specific recommendation in respect of the time interval can be made.
Cholelithiasis
Physiological changes
which occur in the gall bladder following truncal vagotomy for peptic ulcer
disease may contribute to the formation of gall stones.
Anemia if caused by peptic ulcer
disease.
Incisional hernias
Osteoporosis
Total or partial
gastrectomy may result in faulty absorption of essential food stuffs such as
vitamins and mineral salts. Carcinoma of the stomach (in association with H. pylori infection) There is some
epidemiologic evidence supporting an association between chronic H. pylori infection and gastric cancer
(gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma).
The International Agency for Research on Cancer has classified H. pylori as a Group I (definite)
carcinogen in humans. However, the development of gastric cancer is felt to be
multifactorial.
Carcinoma of the stomach (in association
with surgical treatment)Persons who have undergone gastrectomy for benign
disease are at increased risk of developing adenocarcinoma fifteen or more
years after gastrectomy. This finding is particularly relevant in cases of
subtotal or near total gastrectomies.
Therapy
For Peptic Ulcer Disease
Overview
Most peptic ulcers heal
if gastric acid production is adequately suppressed. The rationale behind the
treatment of peptic ulcer disease is two fold. The reduction of hostile factors
is essential, as is augmentation of protective factors. Antacids,
histamineH2-receptor antagonists, proton pump inhibitors (e.g., omeprazole, lansoprazole),
and surgery succeed by neutralization or reduction of gastric acid. Sucralfate
and prostagl and inagents boost mucosal protection. The eradication of H. pylori infection restores normal
mucosal resistance, but unlike other treatment options, does not require
maintenance therapy to prevent ulcer recurrence. Patients should avoid factors
known to contribute to peptic ulcer disease, such as NSAIDs and smoking.
Medical
Therapy
The goal of therapy for
peptic ulcer disease is to relieve symptoms, heal craters, prevent recurrences,
and prevent complications. Medical therapy should include treatment with drugs,
and attempt to accomplish the following:
1) reduce gastric acidity
by mechanisms that inhibit or neutralize acid secretion,
2) coat ulcer craters
to prevent acid and pepsin from penetrating to the ulcer base, 3) provide a
prostagl and inanalog,
4) remove environmental
factors such as NSAIDs and smoking, and
5)reduce emotional
stress (in a subset of patients).
Antacids neutralize
gastric acid and are more effective than placeboin healing gastric and duodenal
ulcers. However, antacids have to be taken in relatively large doses 1 and 3
hours after meals and at bedtime, and may cause side effects. The major side
effect of magnesium-containing antacids is diarrhea caused by magnesium
hydroxide. HistamineH2-receptor antagonists reduce gastric acid production by
blocking the H2 receptor on the parietal cell). Examples of available H2
blockers used to treat gastric and duodenal ulcers include cimetidine,
ranitidine, famotidine and nizatidine. This group of compounds effectively
decreases acid secretion. H2-receptor antagonists are relatively safe. The
choice of drug should be dictated by cost, dosing schedule, convenience, and
possible drug interactions.
The family of drugs
known as as proton pump inhibitors, or PPIs, inactivates the parietal cell hydrogen-potassium
ATPase located on the lumenal surface. ATPase acts as a proton pump and
constitutes the final common pathway in the secretion of hydrogen ions. This
class of medicines is now considered the gold standard in medical therapy of
peptic ulcer disease. Examples of available PPIs include omeprazole,
lansoprazole, pantoprazole, rabeprazole, and esomeprazole. Increasing the PPI
dose can reduce acid secretion to the point of achlorhydria(unachievable by H2
blockade). Thus, the proton pump inhibitors are the primary treatment when gastric
hyper-secretion is resistant to other therapies. Proton pump inhibitors have
been shown to prevent NSAID-associated gastroduodenal ulcers, and to provide a safe
and effective form of therapy. Furthermore, studies have shown that PPIs are
more effective than H2-receptor antagonists at treating all types of peptic
ulcer disease.
Sucralfate is the
aluminum salt of a sulfated disaccharide. The drug forms a barrier or coating
over the ulcer crater, stimulates prostagl and in synthesis, and binds to noxious
agents such as bile salts. Although the exact mechanism of action is unclear,
it appears sucralfates stimulate prostaglandins, which promote improved mucosal
integrity and enhance epithelial regeneration. Because it requires multiple
doses per day, patients are less likely to follow a sucralfate regimen even
though it has been shown to be as effective as an H2 blocker in healing both
duodenal and gastric ulcers. Sucralfate is not absorbed systemically, and its
only remarkable side effect is constipation.
Misoprostol is a
prostaglandinE1 analog that increases mucosal resistance and inhibits acid
secretion to a minor degree. Misoprostol has been advocated for prophylaxis of
NSAID-induced mucosal injury. The drug has significant side effects, primarily
mild to moderate diarrhea, and is too costly to be used by most patients on
long-term NSAIDs.
The suppression of
gastric acid production promotes the healing of peptic ulcers. Unfortunately,
if acid suppression therapy is not maintained, peptic ulcers regularly recur.
Since the long-term cure of peptic ulcers accompanies the eradication of H. pylori, all ulcers associated with
this infection should be treated with the aim of infection eradication.
Although H. pylori is sensitive to a
variety of antibiotics in vitro, its habitat beneath the gastric mucosa makes
it difficult to treat. The original treatment gold standard was 2 weeks of
triple therapy, including bismuth, tetracycline or amoxicillin, and
metronidazole. Where compliance with this regimen can be assured, H. pylori cure rate is 90–95% or more;
however, 20% of these cases develop side effects. Newer simpler regimens have
been developed and H. pylori treatment
recommendations are still evolving. Today, the current gold standard of therapy
is a triple combination of drugs that includes a PPI (e.g. omeprazole or
lansoprazole) plus amoxicillin and a newer antibiotic, clarithromycin. All three
medicines are to be taken twice per day for 7-14 days (preferably 14 days).
Alternative drugs may be offered to those patients with certain allergies or
medication intolerances. Physicians should always offer patients with peptic
ulcer disease and confirmed H. pylori infection
the option of curative therapy. Gastric ulcers should be re-evaluated by
multiple endoscopic biopsies and cytology to rule out gastric carcinoma if they
have not healed after 8 weeks of conventional medical therapy. If no malignancy
is seen on biopsy, aggressive treatment should be instituted for 6 weeks to
eradicate H. pylori and to suppress
acid with full doses of a proton pump inhibitor. A gastric ulcer that does not
heal after this second aggressive course of medical therapy may suggest
underlying malignancy, even with negative repeat biopsies. Non-healing gastric ulcers
should be resected surgically.
Surgical
Therapy
Over the past few
decades in the United States, we have witnessed a declining need for surgery to
treat peptic ulcer disease. This decline may be explained primarily by the
widespread use of H2 receptor antagonists, and now more recently, proton pump inhibitors.
Complications such as gastrointestinal hemorrhage, perforation, or gastric outlet
obstruction remain the major indications for surgical intervention.
The most common reason
for surgical intervention for benign gastric ulcers is failure of the ulcer to
completely heal after an adequate trial of medical or endoscopic therapy.
Patients are usually given a 6-month trial of anti-secretory agents prior to
surgical consultation. The major concern regarding non-healed ulcers is the
high risk of underlying malignancies.
Due to the benign nature
of duodenal ulcers, physicians can monitor the patients’ response to medical
regimens by following their symptoms. When patients with duodenal ulcers
require surgery, it is usually one of three procedures: vagotomy, vagotomy with
antrectomy, or subtotal gastrectomy . Vagotomyalone (without gastric resection)
may involve truncal vagotomy with drainage, selective vagotomy with drainage,
or proximal gastric vagotomy alone (without a drainage procedure). Delayed
gastric emptying may be caused by truncal vagotomy , and a concurrent drainage
procedure such as antrectomy, pyloroplasty, or gastroenterostomy may be
necessary as antral innervation (by Latarjet nerves) is nonfunctioning.
Selective vagotomy(proximal gastric vagotomy) does not necessitate a
concomitant drainage procedure.
Morbidity resulting
from the surgical procedure and the risk of recurrence of ulcers are two major
considerations. Proximal gastric vagotomy is probably the most preferred of
surgical options because the pylorus is preserved. Recurrence of ulcer disease
is about the same with all three types of surgical procedures, however, the
incidence of dumping symptoms is higher with vagotomy or vagotomy with
antrectomy.
Endoscopic
Therapy
The primary role of
endoscopic therapy in peptic ulcer disease is to manage complications that may
arise.
Overview
Hemorrhage,
perforation/penetration, and gastric outlet obstruction continue to be the
major complications associated with peptic ulcer disease, despite the availability
of effective ulcer medications. In the United States, the yearly complication
rate ranges between 2–5%.
Hemorrhage
Rate
of Incidence
Gastrointestinal
hemorrhage affects 5–20% of patients (more often those with duodenal ulcers)
and is the most common complication of peptic ulcer disease. Bleeding occurs
more often in men than in women. Hemorrhage from ulcers stops spontaneously in
approximately 75–80% of cases. Approximately one-fourth of all bleeding ulcers
require surgery.
Endoscopic
Therapy
Endoscopy is the
preferred procedure for the diagnosis and treatment of an upper
gastrointestinal hemorrhage because of the low complication rate and accuracy. Stigmata
on ulcers may be seen during endoscopic procedures, and are important
prognostic indicators. After resuscitation and stabilization of the patient,
gastric lavage is usually performed to remove blood from the stomach prior to
endoscopy. The goal of endoscopic therapy is to “seal” the feeding vessel, and
this may be accomplished in a variety of ways. The bleeding source is
identified in more than 95% of patients with significant upper GI hemorrhage.
Thermally
Active Methods
Thermal devices are the
most widely tested modalities for endoscopic hemostasis. Heating leads to
edema, coagulation of tissue proteins, and contraction of arteries. Heat may be
produced by tissue absorption of laser light energy, passage of electrical
current through tissue, or heat diffusion from another source. Arterial
coagulation is achieved
with the laser by means of rapid heating. The laser is effective for direct
coagulation of 0.25-mm arteries and becomes less effective with larger arteries.
The BICAP, or bipolar circumactive probe, is a thermally active contact or
heater probe used to compress the target artery before heat delivery. After the
initial compression, the delivery of a small amount of heat welds the vessel
walls together. Photocoagulation can be achieved by use of the laser. The laser
light can be focused on a bleeding point to induce rapid tissue heating. This
produces blood coagulation and tissue necrosis. Endoscopic hemostasis may be
achieved with two types of lasers: argon and Nd:YAG. The Nd:YAG laser has
longer wavelengths, greater coagulation capacity, and increased perforation
potential. Both lasers have been used in the endoscopic treatment of ulcer
hemorrhage.
Clinical trials of
ulcer hemorrhage have confirmed that photocoagulation provides effective
hemostasis for active and non-bleeding visible vessels. The success rates with
Nd:YAG are in the range of 80–100%. Important considerations that limit
emergency laser hemostasis include portability and cost. Additionally, the need
for specific expertise by the endoscopist and technician, special electrical
outlets, eye protection, and technical considerations (difficulty in aiming the
laser beam) are further limiting factors in emergency situations.
Electrocoagulation
Heat generated from
high-frequency electrical current is capable of coagulating or cutting tissue.
Thermal electrocoagulation is the classic treatment for bleeding during surgery
and has recently been used endoscopically to treat GI bleeding. Monopolar and
multipolar endoscopic electrodes are currently available, and both must contact
the mucosal surface to be effective.
The multipolar
electrocoagulation probe has two or more electrodes at the tip. Current is
concentrated much closer to the tip than in the monopolar probe, resulting in less
depth of tissue injury and lower perforation potential. The BICAP features six
electrode plates in the tip, a central irrigation channel, and two different
diameter probes. It can achieve a maximum temperature of 100oC and causes less
tissue injury than the monopolar or Nd:YAG electrocoagulation laser.
Heater
Probe
The heater probe is a
hollow aluminum cylinder with an inner coil. The cylinder transfers heat from
its end or sides to tissue when positioned perpendicularly or tangentially.
This probe may be passed through the biopsy channels of larger endoscopes and
positioned on bleeding lesions to produce tamponade and heat Studies have shown the heater probe to be safe
and effective for the treatment of ulcer bleeding or non-bleeding visible vessels,
achieving hemostasis and significantly improving clinical outcomes. In a
comparative study of the heater probe, BICAP, and medical therapy, the heater
probe was more than95% effective in achieving initial hemostasis. Both the BICAP
and heater probes represent important endoscopic advances in endoscopic
hemostasis, and have advantages over laser therapy. These devices are less expensive,
portable, easy to use, have target irrigation, and allow tamponade and
tangential coagulation.
Injection
Therapy
Injection therapy for
upper gastrointestinal bleeding is inexpensive, simple and widely used. A
sclerotherapy catheter with a small retractable needle is passed through the
biopsy channel of the endoscope. Non-bleeding visible vessels are treated by
the injection of a solution at three or four surrounding sites about 1-3 mm from
the vessel. Subsequently, the visible vessel is injected. In cases of bleeding
vessels, injections are made around the bleeding point until hemostasis is
achieved. This is followed by injection into the vessel. Several different
sclerosant agents have been used alone or in combination to achieve endoscopic
hemostasis. Adrenaline; hypertonic saline and adrenaline combined; adrenaline
and polidocanol; pure ethanol;or combinations of dextrose, thrombin, and sodium
morrhuate have shown improvement in rebleeding, the need for urgent surgery,
and mortality. Combined injection and thermal treatment have theoretical
advantages in the treatment of bleeding ulcers. Injection with epinephrine
produces vasoconstriction and activates platelet coagulation, reducing blood
flow and potentiating thermal therapy, which produces coaptive coagulation.
Recent studies have shown combination therapy (epinephrine injection and heater
probe) benefited patients with spurting bleeding, but not those with oozing
bleeding.
Mechanical
Therapy
Endoscopic hemoclips
have recently been developed and made their way to the scene of endoscopic
therapy for peptic ulcer disease. These devices are small3-4 mm titanium clips
that can be opened and closed while being operated through the working channel
of the endoscope. They may be used to pinch-off, or clip, a bleeding vessel.
When fully deployed, they remain fastened to the vessel after the endoscope has
been removed from the patient. Emerging studies have shown that hemoclips are
an effective and safe method for treating certain forms of peptic ulcer desease
and should be used in the appropriate setting.
Radiological
Therapy
Angiography is a useful
diagnostic and therapeutic modality in treatment of bleeding gastric and
duodenal ulcers. Angiography can identify the site of bleeding in instances
where endoscopy has failed to be diagnostic. It should also be considered in
patients at high risk for surgical intervention.
Angiographic therapy
includes two different embolization techniques for the treatment of GI
bleeding. Effective in 50% of cases, vasopressin intra-arterial infusion causes
vasoconstriction that results in the cessation of ulcer hemorrhage. Embolic
material such as an absorbable gelatin sponge, tissue adhesives, or other occlusion
devices (such as microcoils) can be inserted through a catheter into the area
of bleeding. Potential complications of embolization therapy may include
ischemia and perforation.
Surgical
Therapy
When endoscopic
hemostasis techniques are unavailable or fail to resolve bleeding or recurrent
hemorrhage, surgery provides another therapeutic option. Surgery is effective
in the prevention of recurrent ulceration and in excluding the presence of
malignant disease. Emergent surgery has a higher mortality rate than elective
surgery, and resection procedures are accompanied by higher mortality than over
sewing the ulcer and selective vagotomy, or vagotomy and pyloroplasty. The
operative choice is related to the surgeon’s experience, ulcer location, and
overall condition of the patient. Truncal vagotomy and antrectomy provide high cure rates and low recurrence
rates. Recurrence rates after vagotomy and pyloroplasty are somewhat higher. Laparoscopic
selective vagotomy provides an appealing alternative for a subset of ulcer
patients with lower morbidity, shorter recovery time, and a shorter hospital
stay.
Perforation
Approximately 5–10% of
patients with peptic ulcers suffer a perforation into the abdominal cavity. This
rate is higher in men than in women. Approximately 15% of patients die from
ulcer perforation.
Two types of
perforation of the stomach and duodenum have been observed. Free perforation
occurs when duodenal or gastric contents spill into the abdominal cavity with
peritoneal contamination by gastric, pancreatic and biliary juices. Clinically
this produces an acute abdomen, which is easily diagnosed. Contained
perforation occurs when
the ulcer produces a full-thickness hole in the duodenum or stomach, but the
omentum or other adjacent organs prevent peritoneal contamination.
Perforations are most
likely in elderly patients onchronic NSAID therapy, and are more common in
gastric than in duodenal ulcers. Initial symptoms of perforated duodenal or
gastric ulcers include severe abdominal pain, worse in the epigastrium, often
accompanied by nausea and vomiting. Typically the patient is acutely and severely
ill. History and physical exam suggest a diagnosis of perforation. The finding
of free air on either an upright or decubitus abdominal radiograph is noted in approximately
70% of cases.
An upper GI series with
gastrografin will confirm the clinical impression of perforation if an x-ray is
negative. Perforation is a contraindication for endoscopy because air
insufflation may exacerbate spillage of gastric contents or disrupt a sealed
perforation. Urgent surgical therapy is recommended in patients with
uncontained, free perforated ulcers, because spontaneous sealing is rare. In
addition, gastric adenocarcinoma cannot be ruled out and there is a greater
potential for bacterial colonization. Aggressive surgical intervention helps to
decrease the high mortality associated with perforating gastric ulcers.
Penetration
Five to 10% of
perforating ulcers may erode through the entire thickness of the gastric or
duodenal wall into adjacent abdominal organs. Such penetration can involve the
pancreas, bile ducts, liver, and the small or large intestine. The pancreas is
the most common site of penetration.
The acute onset of
associated complications, such as pancreatitis, cholangitis, or diarrhea of
undigested food, may diagnose penetration. The diagnosis of penetration is more
difficult than perforation, and is based on a combination of severe ulcer
symptoms, atypical pain distribution, and diminished response to the usual therapy.
Surgery is usually not recommended in the management of penetration unless
biliary complications are present or the underlying peptic disease is severe.
Gastric
Outlet Obstruction
Fewer than 5% of
patients develop gastric outlet obstruction from pyloric stenosis. Duodenal
ulcers give rise to pyloric stenosis more often than gastric ulcers. Peptic ulcer
disease may be accompanied by varying degrees of obstruction caused by
inflammatory swelling of the pyloric channel or chronic scarring associated
with fibrosis.
Patients with gastric
outlet obstruction usually have a history of nausea, vomiting, and epigastric
pain or fullness. Laboratory findings may show anemia, low serum albumin, and
hyperkalemic alkalosis. Radiological exam is usually diagnostic, showing a
large gastric shadow with an air/fluid level. An upper GI series yields
valuable information by showing marked delaying gastric emptying and a large atonic
stomach. Endoscopy is the best test for evaluating gastric outlet obstruction
after decompression of the stomach for 12–24 hours.
Endoscopic
Therapy
Endoscopic dilation of
the gastric outlet obstruction is a reasonable course after the failure of medical
therapy. Balloon dilation can usually improve the acute problem by producing
radial forces on the strictured segment. Through-the-scope balloons are usually
the first choice (over guide wire balloons), using the largest balloon that
can safely be passed
into the segment. A well-lubricated balloon is passed through the endoscopic
biopsy channel and carefully positioned into the stricture. The balloon is
inflated with contrast, water or air, and pressure is maintained for the
desired time. Dilation may also be performed over a guide wire that has been
passed through the stricture. Sequential balloon dilation is performed with
fluoroscopy and endoscopic evaluation.
Surgical
Therapy
The goal of surgical
therapy in gastric outlet obstruction is two fold:
1) improvement of the obstruction and
2) treatment of the predisposing ulcer with an
acid-reducing procedure. Vagotomy and antrectomy with gastroduodenal drainage,
or truncal vagotomy with drainage are the recommended surgical
procedures. Selective vagotomy
with pyloroduodenal dilation is an alternative, but recurrent obstruction rates
arehigher than with the other two surgeries.
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