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COMPLICATIONS OF GASTRO-DUODENAL PEPTIC ULCERS
Approximately one of three patients with peptic ulcer disease experiences
bleeding, perforation or obstruction at some point in the course of the
disease.
Perforation, bleeding and stenosis are usually complications of a chronic
symptomatic ulcer, but each can occur with little or no previous history.
These complications increase the morbidity and mortality of peptic ulcer
disease.
Perforation
Perforation is ulcer rupture into the peritoneal cavity with spillage of gastroduodenal contents.
Penetration is an erosion into a solid organ such as pancreas or liver.
Free perforation into the general peritoneal cavity is a catastrophic event, the
signs and symptoms of which do not usually cause diagnostic problems.
When perforation of a chronic ulcer occurs there will often have been an
increase in the severity of the dyspepsia for a few days prior to the
perforation.
When an acute ulcer perforates there may be no premonitory symptoms,
particularly in younger patients.
Steroid-induced perforations undoubtedly occur, but the etiology is not
straightforward. For instance, perforation is much more common in patients
with rheumatoid arthritis on steroids than in patients with ulcerative colitis.
The use of non-steroidal anti-inflammatory drugs (NSAID) has been shown
to be associated with an increase incidence of peptic ulceration and with a
increased risk of complications of both perforation and bleeding.
Acute perforations also accompany situations of stress such as burns,
multiple injuries, sepsis and in patients receiving intensive chemotherapy
and radiotherapy.
Perforation of malignant gastric ulcers is common and although most
perforated gastric ulcers will be benign, biopsy at the time of operation is
important if the ulcer is not removed.
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Clinical features
The moment of perforation is often identified by the patient as an
excruciating epigastric pain. The subsequent symptoms depend in part on the
degree of peritoneal soiling and whether or not the perforation becomes
sealed. The pain may become generalized. In addition, it may be felt over
the shoulder if diaphragmatic irritation ensues.
Sometimes the spread of gastroduodenal content is maximal along the right
paracolic gutter so that pain may localize to the right iliac fossa and simulate
appendicitis.
Significant vomiting is uncommon unless the diagnosis is delayed and an
ileus becomes established.
The physical signs accompanying perforation will again depend upon the
degree and rate of soiling.
Tenderness with guarding may vary from being localized to the upper
abdomen to being generalized.
If contamination of the general peritoneal cavity has occurred there will
usually be rigidity and a silent abdomen with progressive distention as a
later feature. A variable degree of circulatory collapse may be present with
tachycardia, hypotension, a cold periphery and a decreased urinary output.
Respiration will often be shallow, any deep inspiration provoking increased
pain. The patient lies still in the bed, any movement exacerbating the pain.
Diagnosis
The key to the diagnosis, suspected from the signs and symptoms, is the
plain abdominal X ray taken in the erect position. Although free peritoneal
gas may come from any of the digestive hollow organs, in practice the
finding of subdiaphragmatic air is pathognomonic of gastroduodenal
perforation.
Radiological features of an ileus may be present in more advanced cases.
If a pneumoperitoneum is not seen radiologically, the diagnostic problem is
to differentiate between a sealed perforation with minimal localized soiling
and an acute pancreatitis.
In the absence of a pneumoperitoneum a serum amylase estimation should
be performed. If doubt persists an USS of the abdomen or a diagnostic
peritoneal lavage may help.
Management
Initial treatment should be directed toward correction of hypovolemia and
any electrolyte imbalance.
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Oliguria and poor peripheral perfusion are contraindications to immediate
operative treatment and their correction should take precedence even over
radiological studies.
If necessary, resuscitation should be monitored with measurement of central
venous pressure and urine output from a urinary catheter.
Colloids can be used for resuscitation, but cristaloids in term of a balanced
salt solution is equally effective.
Nasogastric aspiration should be instituted.
Antibiotics are not recommended routinely since the initial peritonitis is
chemical.
Operative or Conservative Treatment
There is no doubt that many patients with perforated ulcers can be managed
non-operatively with initial success.
A policy of naso-gastric suction, intravenous fluids, antibiotics and
antisecretory drugs will allow some perforations to seal spontaneously and
the ileus to resolve.
This conservative approach is called Taylor’s method and implies a close
clinical observation ( temperature, physical examination of the abdomen)
and lab. tests ( FBC) and abdomen USS monitoring.
The problem with this approach of management is that there is a high
incidence of residual abscess formation, particularly in the subphrenic region
which will subsequently require drainage.
The likelyhood of therapeutic success with this method, increases in young
patients with short history of the disease.
An operative approach is advisible if the patient does not respond to this
after a period of 6-12 hours of correct treatment.
One purpose of laparotomy is to aid in sealing the perforation and then to
perform a thorough peritoneal cleansing. The quickest method of dealing
with the perforation is simple closure.
Closure is achieved by inserting sutures which transfix the entire thickness
of the stomach wall. The sutures are inserted in the long axis of the gut to
avoid narrowing of the lumen. The sutures are tied over a piece of omentum.
Before the abdominal wound is closed the entire peritoneal cavity should be
washed out with as much warm saline as is required to produce a
completely clear effluent. This requires 3-4 l. of fluid. Particular attention
should be paid to the subphrenic areas and pelvis.
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Pyloric stenosis
Pyloric stenosis is in fact, rarely due to stenosis at the pylorus. More
commonly, the site of the obstruction is on one side or the other of the
pylorus- either the duodenum at the site of chronic scarring from ulceration
or the antrum where a benign ulcer or a cancer is a problem.
True pyloric stenosis can arise from a pyloric channel ulcer or very rarely
from an adult hypertrophic pyloric stenosis.
Clinical features
Pyloric stenosis usually occurs in a patient with longstanding symptoms of
ulcer disease. A short preceding history with little in the way of
characteristic ulcer pain suggests that the obstruction may be malignant.
As obstruction develops, however, the character of pain may change to
become more of a generalized upper abdominal discomfort.
Vomiting and anorexia supervene. As vomiting increases, pain may become
less of a feature. The typical vomiting of pyloric stenosis is effortless and
projectile and the vomitus is characterized by an absence of bile and the
presence of partially digested food eaten hours or even days previously.
With repeated vomiting and failure to eat, the patient often becomes
constipated. Examination will usually show an underweight patient,
dehydrated and often with a degree of anemia. In advanced cases there will
be evidence of gastric stasis in the form of a succusion splash.
Visible peristalsis may be apparent, passing across the upper abdomen from
left to right and the dilated stomach may actually be palpable.
Metabolic features
Prolonged vomiting of gastric contents results in a characteristic series of
electrolyte disturbances.
Initially, the major loss is fluid rich in hydrogen and chloride ions so that a
degree of dehydration may accompany a hypochloremic alkalosis. At this
stage the serum sodium is usually normal and hypokalemia may not be
obvious.
The more marked metabolic changes which accompany unrelieved outlet
obstruction result from a combination of continued losses with secondary
changes in renal function.
In the early stages the urine is characterized by a low chloride content and is
appropriately alkaline because of enhanced bicarbonate excretion. This tends
to compensate for the metabolic alkalosis, but it does so at the expense of
losing sodium.
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If the gastric losses continue the patient thus becomes progressively more
dehydrated and hyponatremic.
In an attempt to conserve circulating volume, sodium is retained by the
kidneys and hydrogen ions and potassium are excreted preferentially. At this
late stage, therefore, the patient with a metabolic alkalosis will have a
paradoxically acid urine.
Hence the alkalosis becomes more severe and hypokalemia is more marked.
As a secondary effect of the alkalosis, the concentration of plasma-ionized
calcium may fall so that disturbances of conscious level and tetany may be
apparent. These electrolyte disturbances encountered in patients with severe
pyloric stenosis are termed Darrow syndrome in which the lab.findings are:
high base excess (alkalosis), high serum urea, low serum sodium, potassium
supplements as indicated by electrolyte determinations.
Provision of adequate sodium allows excretion of alkaline urine so that the
alkalosis becomes correctable. Success is indicated by clinical improvement
in the state of hydration, by an increase in urine output, a fall to normal in
blood urea and hematocrit and restoration to normal of electrolyte
concentrations. Gastric lavage should be performed with a wide-bore tube
using saline for irrigation. This should be performed twice daily initially and
until returning fluid is quite clear.
The patient should not be allowed to eat, but fluids may be given and milky
drinks should be encouraged.
One benefit of bed rest, rehydration, lavage and milk drinks is that an ulcer
will begin to heal and with subsidence of the inflammatory changes the
obstruction will begin to remit.
Such improvement is often apparent even when the cause of the obstruction
is a malignancy. This stage of management will often take a week or more.
The object is to get the patient into the best possible state for surgery, and it
is a mistake to accept less that this ideal.
Occasionally, provision of adequate nutrition will require intravenous
feeding. It may be difficult to make a firm clinical diagnosis of the cause of
the pyloric stenosis. Even when the stomach has been well prepared,
radiological studies may merely confirm outlet obstruction and fail to reveal
the cause.
Gastroscopic examination with biopsy is appropriate once the stomach is
cleansed. The definitive treatment for pyloric stenosis in fit patients is partial
gastric resection with gastro-duodenal anastomosis ( Pean-Bilroth I ) or
closure of the duodenal stump, gastro-jejunal anastomosis ( Reichel-Polya ).
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In old frail patients a by-pass operation like gastro-jejunostomy which takes
less operative time than a partial resection is appropriate.
Balloon dilatation is an option for surgically unfit patients.
Bleeding Peptic Ulcer
Acute bleeding is the commonest complication of peptic ulcer. It occurs in
5%-15% of all patients with gastro-duodenal ulcers and carries the highest
mortality of any of their complication.
Hemorrhage results from erosion of the ulcer into a blood vessel. The most
common sign of acute bleeding is melena with or without hematemesis.
Risk of bleeding is unrelated to duration of ulcer disease, one of three
patients have no history of ulcer disease when he or she presents with
bleeding.
In some patients with major hemorrhage, gastrointestinal transit of blood
may be so rapid that the stool is bright red. Moreover a naso-gastric aspirate
may not contain blood if active bleeding from a duodenal ulcer does not
reflux into the stomach.
The hemoglobin and hematocrit on admission may not reflect the severity of
bleeding if sufficient time has not elapsed to allow for compensatory
hemodilution, therefore the severity of acute bleeding is better assessed by
the blood pressure and pulse rate. A systolic BP of less than 100 mm.Hg.
and a pulse rate of more than 100 beats per minute, both taken with the
patient supine, suggest major blood loss (more than 1000 ml.).
The differential diagnosis includes : esophago-gastric varices, hemorrhagic
gastritis, Mallory-Weiss laceration, benign and malignant gastric neoplasms,
vascular anomalies (angiodysplasia), aorto-enteric fistula usually in patients
with a prosthetic aortic graft.
Certain clinical factors may adversely affect clinical outcome in patients
with bleeding peptic ulcer: - severe, continuing bleeding
- early rebleeding within 3-5 days of initial
stabilization
- age greater than 60 years
- associated diseases: cardio-vascular and liver
disease
The diagnostic approach is now generally agreed: the method of choice is
emergency endoscopy at an early stage- this offers a truthworthy means of
locating the sourse of the bleding and ascertaining its activity.
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Forrest’s classification of bleeding activity
Bleeding activity
Endoscopic criteria
Forest I a-active bleeding
arterial bleeding (spurting)
Forrest I b-active bleeding
oozing
Forrest II-bleeding ceased
clot lying on ulcer base/visible
vessel stump
Forrest III- bleeding ceased
lesion with no signs of recent
bleeding
There are three phases in the management of bleeding patient: resuscitation,
diagnosis and definitive treatment.
Resuscitation
The general principles involved in managing hemorrhagic shock are dealt
with in the Intesive Care Unit.
Adequate resuscitation is imperative before any diagnostic measures are
undertaken and there should never be any question of sedating patients for
endoscopy whilst they are still hypovolemic from blood loss.
In less severe cases it may be necessary to do no mare than erect an iv line
as a precaution against a further major bleed, but often rapid transfusion will
be needed. Central venous pressure monitoring and measuring urine output
are invaluable in the severely shocked patient.
Confusion and restlessness demand attention for oxygenation and volume
replacement, not sedation.
Diagnosis
The likely sourse of blood loss may be suggested by clinical features.
A long dyspeptic history, stigmas of chronic liver disease, a recent high
intake of alcohol and perhaps aspirin and other NSAID suggest a chronic
ulcer, varices or erosions as the likely bleeding lesions.
It must be stressed, however, that direct endoscopic visualization of the
esophagus, stomach and duodenum is the only way to make a firm decision
upon which rational management can be planned.
Aside from establishing the cause of bleeding, upper gastrointestinal
endoscopy is extremely valuable in predicting those patients with ulcer
disease who are likely to continue to bleed or develop recurrent hemorrhage.
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The endoscopic stigmata which indicate this eventually and therefore the
need for early surgical intervention are: arterial spurter, identifiable vessel in
the base of ulcer, adherent clot.
Management
Following adequate resuscitation and diagnosis there are a number of
general measures which should be carried out. The patient should be on bed
rest initially and a nasogastric tube passed into the stomach. If clot is present
in the stomach it is useful to remove this with cold saline lavage. A careful
watch is kept for continued or recurrent bleeding, In addition to the passage
of fresh melena or the aspiration of fresh blood from the stomach, continued
blood loss is indicated by the need to give more fluid to maintain
cardiovascular stability.
Hemostatic drugs plus anti H2 receptor drugs given iv are indicated as
medical treatment. Anti H2 receptor drugs not only lower acid secretion but
also appears to have a beneficial action on the gastric mucosal barrier.
Indications for surgery
The role of surgery is twofold: to stop bleeding which it is judged will not
stop spontaneously and to anticipate those cases in which re-bleeding is
either likely or in which a rebleed would carry a significant risk to the
patient.
The criteria for operation thus become:
1. continuing bleeding; if after the initial period of resuscitation,
bleeding continues, surgery is indicated as means of controlling
hemorrhage.
2. re-bleeding; a fresh bleed occurring some hours or days after
apparent cessation of the initial hemorrhage suggests that surgery
should be performed as soon as adequate transfusion has been
accomplished. These patients can often be identified at the initial
endoscopy.
3. the sourse of bleeding; if the endoscopist reports a chronic posterior
wall duodenal ulcer with clot adherent to a large artery, the indications
for operation are stronger than if a hemorrhagic anterior wall ulcer is
all that is seen. Bleeding GU should be operated on promptly since rebleeeding is common and carries a significant risk.
4. fitness of the patient; the presence of severe cardiorespiratory disease
is a significant factor in deciding whether or not to advise surgery. It
is not merely a question of deciding upon the risk of a laparotomy, but
more a matter of assessing the effect that a further bleed would have
on the patient. This is particularly important when cardiac disease is
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present, for a period of hypotension following a gastrointestinal bleed can
be the cause of a myocardial infarction. In general, the older or more ill
the patient, the greater is the indication for early surgery.
In the face of continuing bleeding, the prudent surgeon will make sure that
coagulation parameters are normal before embarking upon surgery. The
difficulty which may arise is that the sourse of bleeding is still unclear even
on a full laparotomy which should include generous gastrotomy and
duodenotomy incisions. Under these circumstances it is quite likely that the
cause of bleeding is one of the uncommon angiodysplasias.
If it is not possible to localize the area of bleeding which by this time may
have stopped, then it can be of great help to have an endoscope passed. With
the theatre lights turned down, the transillumination may show a leash of
abnormal vessels. In addition, the endoscopist may see a mucosal
abnormality. Emergency arteriography will need to be considered if the
patient re-bleeds. Scintigraphy with labeled red cells is another option.
80% of patients with a bleeding ulcer will stop bleeding spontaneously.
The majority of significant bleeds come from posterior penetrating ulcers
which have eroded into the gastroduodenal artery. The presence of fibrosis
in the ulcer base, the presence of an arteriosclerotic artery and clot adherent
to this ulcer or an active arterial spurter at the time of endoscopy makes it
unwise to assume that the patient will stop bleeding or not rebleed.
The goal of surgery for bleeding ulcer is to combine an ulcer operation with
reliable hemostasis. These objectives are accomplished by partial
gastrectomy in which the ulcer area is included.
The morbidity and mortality have prompted many surgeons to adopt the
more conservative approach of underrunning the bleeding ulcer with strong
non-absorbable material.
Underrunning of the bleeding ulcer without vagotomy followed by treatment
with H2-blockers (omeprazole) or proton pump inhibitors (controloc, losec)
has been advocated, particularly in the elderly.
The Failures of Gastric Surgery
Unsatisfactory results follow ulcer surgery in 10-20% of cases. Poor results
may be because of recurrent ulceration, alimentary side-effects or nutritional
disturbances.
Recurrent Ulceration
Recurrent ulceration may appear in the stomach, the duodenum or at the site
of a gastrointerstinal stoma.
Gastric ulceration implies either delayed emptying or duodenal reflux.
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Recurrent duodenal or stomal ulceration suggests that the ulcer diathesis
persists; in other words the hypersecretory state has not been corrected
sufficiently by the previous operation.
The causes of recurrent ulceration are:
1.- incomplete vagotomy; failure to achieve complete denervation of the
parietal cell mass is the commonest cause of recurrent ulceration. The
incidence of incomplete vagotomy may be as high as 20% after truncal
vagotomy as judged by the results of early postoperative insuline tests.
2.- inadequate resection; if gastrectomy is to be the sole means used for
reducing acid secretion a minimum of ¾ of the stomach needs to be
removed.
3.- retained gastric antrum; if residual antral tissue is left in continuity with
the duodenal stump, the antral G cells, now in an alkaline environment will
secrete gastrin continuously. Under this constant stimulus the remaining
parietal cells will produce sufficient acid for stomal ulceration to develop.
4.-Zollinger-Ellison syndrome; this syndrome describes the association of an
intractable ulcer status with a gastrin-secreting tumor, usually in the
pancreas. The rapidity of the return of symptoms and their virulence,
sometimes indicated by perforation or hemorrhage, should raise the
suspicion of this problem.
Because the parietal cell mass is under constant stimulation, the
characteristic finding is of a high level of basal secretion relative to maximal
stimulated secretion. The measurement of plasma gastrin concentrations
confirms the diagnosis.
5.- hypercalcemia; in practice, if hypercalcemia is found in a patient with a
peptic ulcer, recurrent ulcer, parathormone levels should be measured.
If hyperparathyroidism is found and corrected surgically, plasma gastrin
concentrations may fall to normal and the ulcer will often heal.
There is some suggestion that this is more likely to occur if the patient has a
parathyroid adenoma rather than hyperplasia.
If the ulcer persists despite parathyroidectomy and especially if gastrin
concentrations remain elevated evidence for a gastrinoma must be sought.
Management of the Patient with Recurrent “Dyspepsia”
The persistence of indigestion or its return after a period of freedom from
symptoms suggests the possibility of recurrent ulceration.
Fibreoptic endoscopy is the best method for detecting ulcer recurrence and it
may give valuable information if gastritis and/or bile reflux are present.
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A trial of medical treatment with H2-receptor antagonists or proton pump
inhibitors is a reasonable approach to recurrent duodenal or stomal
ulceration.
Recurrent ulceration in the body of the stomach will often respond to
sucralfate and metoclopramide is a useful additional agent.
Ulcer healing under these circumstances was associated with alcohol or
drugs such as aspirine.
If the recurrence does not respond promptly to such measures, further
investigation is required to establish why the ulcer has reappeared.
The usual reason is that the “hypersecrotory” state persists due either to
incomplete vagotomy or inadequate resection.
If vagotomy has been previous operation and investigations indicate
persisting hypersecretion with incomplete vagotomy, revagotomy may be
attempted by the abdominal or thoracic routes. However, it is more prudent
to proceed to antrectomy with revagotomy.
When hypersecretion persists after gastrectomy in the absence of
hypergastrinemia the addition of a truncal vagotomy to what should amount
to at least a hemigastrectomy is usually adequate and safer than a reresection. The differential diagnosis should include retained antrum from a
gastrinoma. Surgical removal of retained antral tissue may not be easy and a
long-term antisecretory drugs should be contemplated.
If the diagnosis of the Zollinger-Ellison syndrome is confirmed than
selective arteriography should be used to demonstrate the blood supply of
the pamcreas. This may demonstrate the tumor. The surgical treatment is
excision of the tumor.
Patients responding poorly to antisecretory drugs and at exploration are
found to have either no tumor or multifocal disease are treated by total
gastrectomy in order to prevent life-threatening peptic ulcer complications.
Study questions
1. Point out the diagnostic criteria in a perforated peptic ulcer and the
treatment modalities in such condition .
2. What are the characteristic clinical features in pyloric stenosis?
3. What is Darrow syndrome?
4. What is the management in a patient with pyloric stenosis with
Darrow syndrome?
5. How would you manage a 70 years old patient who presented with a
first episode of repeated melena, associated with systolic blood
pressure of 80 cm.Hg and pulse rate of 120/min irregular and with no
previous history of peptic ulcer disease .
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