Chapter 5 Peptic ulcer acute haemorrhage

Peptic ulcer acute haemorrhage is a common occurrence throughout the world. In France, a recent report concludes that the mortality from peptic ulcer acute haemorrhage has decreased from about 11 to 7%; however, a similar report from Greece finds no decrease in mortality.

Patients typically present with an ulcer that has bled or is actively bleeding. Approximately 80% of ulcers stop bleeding. The overall mortality rate is approximately 10%. Rebleeding or continued bleeding is associated with increased mortality. Comorbidities increase the probability of rebleeding in patients after endoscopic therapy. An increasing  amount of evidence in the literature states that therapy with high-dose proton pump inhibitors may decrease the rate of rebleeding after endoscopic therapy. By increasing  the gastric pH above 6, the clot is stabilized.

This patient population has become progressively older, with significant comorbidities that increase mortality.

Pathophysiology

Duodenal ulcer disease is strongly associated with Helicobacter pylori infection. The organism causes disruption of the mucous barrier and has a direct inflammatory effect on gastric and duodenal mucosa. Eradication of H pylori has been demonstrated to reduce the risk of recurrent ulcers and, thus, recurrent ulcer haemorrhage.

NSAIDs are the second major aetiology of ulcer haemorrhage because of their effect on cyclooxygenase-1, which leads to impaired mucosal defense to acid. The use of cyclooxygenase-2 inhibitors has been shown to reduce the risk of ulcer haemorrhage, although only when not combined with aspirin therapy. Recent concerns have been raised about an increase in myocardial infarction and stroke in patients taking selective cyclooxygenase-2 inhibitors.

The combination of H pylori infection and NSAID use may increase the risk of ulcer haemorrhage.

As the ulcer burrows deeper into the gastroduodenal mucosa, the process causes weakening and necrosis of the arterial wall, leading to the development of a pseudoaneurysm. The weakened wall ruptures, producing haemorrhage. The flow through the vessel varies with the radius: small increases in vessel size can mean much larger amounts of blood flow and bleeding. Visible vessels usually range from 0.3–1.8 mm.

Massive haemorrhage has been reported from larger vessels. The larger vessels are located deeper in the gastric and duodenal submucosa and serosa. Larger branches of the left gastric artery are found high on the lesser curvature, while the pancreatoduodenal artery and its major branches are located posteroinferiorly in the duodenal bulb.

The size of the vessel is important in the prognosis in that larger vessels cause faster blood loss, with more severe hypotension and more complications, especially in older patients.

The main disturbances in patients with acute peptic ulcer bleeding are:

1. Acute loss of blood leads to rapid reduction of cardiac output.

2. Activation of simpatico-adrenal system results in peripheric vasoconstriction and centralization of blood supply.

3. Mechanisms of compensation are supplemented with haemodilution (displacement of interstitial liquid into vessels) and increasing  of aldosterone production).

4. After loss less 20% of volume of blood circulation the bleeding stops and in absence of haemorrhagic compensation the disturbances of circulation of blood are not observed.

5. After loss more 20% of volume of blood circulation without the proper compensation of haemorrhage such patients can survive, however always there are considerable disturbances of blood circulation with disturbance of functions of liver and kidneys.

6. Inadequate peripheric blood supply leads to hypoxia, stimulates anaerobic glycolysis and results in free radical metabolites (metabolic acidosis).

7. Reological disturbances result in embolism and thrombosis in microcirculation bloodstream.

8. Arteriovenous shunts open, multiple organ failure develops (“sock” lungs, kidneys, liver).

9. Loss of blood cells results in immunodeficiensy.

Classifications

Stages of blood loss (Shalimov A. A., 1987)

20% of volume of blood circulation.

20–30% of blood circulation.

More than 30% of blood circulation.

Forrest endoscope classification

(Forrest J. A. H., 1974)

Forrest I. Active bleeding.

Forrest II. Temporary haemostasis. Ulcer is covered with haematin, thrombus, blood clot (risk of bleeding recurrence 40%).

Forrest III. There aren’t signs of bleeding (risk of bleeding recurrence is 4%).

History

It is needed to remember, that anamnesis is very important for diagnosis. The patient history findings include weakness, dizziness, syncope associated with haematemesis (coffee ground vomitus), melena (black stools with a rotten odour) and haematochezia (red or maroon stool).

More patients tell about their peptic ulcer disease. Sometimes bleeding has occurred repeatedly or patients have undergone surgery for perforated ulcer in the past. In some patients a gastric or duodenum ulcer was not diagnosed before and correctly collected anamnesis revealed that the patient had stomach ache. Patients often tell that pain in upper part of abdomen which occurred a few days prior to bleeding, suddenly disappears the onset of bleeding (Bergmann’s sign).

Patients may have a history of previous dyspepsia (especially nocturnal symptoms), ulcer disease, early satiety, and NSAID or aspirin use. Many patients with peptic ulcer acute haemorrhage who are taking nonsteroidal anti-inflammatory drugs present without dyspepsia but with haematemesis or melena as their first symptom. Low-dose aspirin (81 mg) has been associated with peptic ulcer acute haemorrhage with or without the addition of NSAID therapy. Patients with a prior history of ulcers are at an especially increased risk for peptic ulcer acute haemorrhage when placed on aspirin or NSAID therapy and should receive continuous acid suppression with a proton pump inhibitor. Because recurrence of ulcer disease is common, history findings are relevant.

Patients may present in a more subacute phase with a history of dyspepsia and occult intestinal bleeding manifesting as a positive faecal occult blood test result or as iron deficiency anemia.

A history of recent aspirin ingestion suggests that the patient may have nonsteroidal anti-inflammatory drug gastropathy with an enhanced bleeding diathesis from poor platelet adhesiveness.

A history of chronic alcohol use of more than 50 g/d or chronic hepatitis (B or C) increases the risk of haemorrhage, gastric antral vascular ectasia, or portal gastropathy.

The presence of postural hypotension indicates more rapid and severe blood loss.

Clinical manifistation

In patients with peptic ulcer disease bleeding starts mainly at night. Vomiting can be the first sign, mostly, with gastric localization of ulcers. Vomiting, as a rule, is “coffee-ground” in appearance. Sometimes it is with fresh blood or blood clots.

The black stool is the permanent symptom of ulcer bleeding, with an unpleasant smell (“melena”) that can take place few times in day.

Bloody vomiting and “melena” is accompanied by worsening of the general condition of patient. An acute weakness, dizziness, noise in a head and darkening in eyes, sometimes – loss of consciousness. A collapse with the signs of haemorrhagic shock can also develop.

In patients with ulcer bleeding there are typical changes of homodynamic indexes: the pulse is rapid, weak filling and tension, arterial pressure is mostly reduced. These indexes need to be observed in the dynamics, as they can change during the short interval of time.

There is pallor of skin and visible mucosas at an examination. The stomach sometimes is moderately enlarged, but more frequently it is pulled in, soft on palpation. In upper part it is possible to notice hyperpigmented spots – as a result of prolonged application of hot-water bottle. Pain on deep palpation in the region of right hypochondrium (duodenal ulcer) or in a epigastric region (gastric ulcer) is often observed in penetrated ulcers. Mendel’s sign – pain on percussion in the projection of piloroduodenal region – may be indicated.

In the examination of patients with the gastrointestinal bleeding digital examination of rectum is obligatory. It needs to be performed at the first examination, because information about the presence of black excreta (“melena”) is important. In addition, it is sometimes possible to expose the tumour of rectum or haemorrhoidal nodes which are also the source of bleeding.

Clinical variants

It is necessary always to remember that complication of peptic ulcer by bleeding happens considerably more frequently, than it is diagnosed. The clinical signs and staging of disease depends on the degree of blood loss. Usually, 50–55% of moderate bleeding (microbleeding) are unseen. In fact profuse bleeding with the loss of 50–60% of the volume of circulatory blood could stop the heart and cause the death of patient.

For loss of 20% of volume of blood circulation (I stage) typically: rabid pulse rate to 90–100 per min., decreasing  of arterial blood pressure to 90/60 mm Hg. The excitability of patient changes by lethargy, however consciousness is clear, breathing is frequent. After the bleeding stops and in absence of hemorrhagic compensation the disturbances of circulation of blood are not observed.

In patients with the II stage of haemorrhage (loss of  20–30% of blood circulation) the general condition needs to be estimated as average. Expressed pallor of skin, sticky sweat, lethargy. Pulse rate – 120–130 per min., weak filling and tension, arterial blood pressure – 90–80/50 mm Hg. In the first few hours the spasm of vessels (centralization of blood circulation) arises after bleeding. Without the proper compensation of haemorrhage such patients can survive, however always there are considerable disturbances of blood circulation with disturbance of liver and kidneys functions.

The III stage of haemorrhage (more than 30% of blood circulation). The pulse rate in such patients is 130–140 per min., and arterial blood pres­sure – from 60 to 0 mm Hg. Consciousness is almost always darkened, adynamy is acutely expressed. Central vein pressure is low. Oliguria is observed, that can change to anuria. Without active and directed correction of haemorrhage the patient can die.

Amount of bleeding doesn’t always correspond to the general condition of patient. It can depend on compensatory mechanism of the organism, rate of loss of blood and the presence of accompanying pathology.

It is needed to remember, that the ulcer bleeding can accompany the perforation of ulcer. During perforation, ulcers are often accompanied by bleeding. Correct diagnosis of these two complications has important value in tactical approach and in the choice of method of surgical treatment. In fact simple suturing of perforated and bleeding ulcer can lead to complica­tions in the postoperative period, as profuse bleeding and cause the neces­sity of repeat operation.

Differential diagnosis

With wide use of gastroduodenoscopy the question of differential diagnosis of bleeding is less significant. However such a problem arises due to impossibility to use this method of examination when the general condition of patient is bad or taking into account other reasons. Differential diagnosis is conducted in bleeding of nonulcer origin, which can arise in different parts of digestive tract.

For bleeding from the varicose veins of esophagus in patients with portal hypertension with liver cirrhosis. This type of bleeding is massive and leading to considerable haemorrhage. Vomiting of fresh blood, expressed tachycardia, falling of arterial pressure are observed. In such patients it is possible to find the signs of cirrhosis of liver and portal hypertension.

The cancer of stomach in the destruction stage can be also compli­cated by bleeding. Such bleeding often are not massive, and chronic character is carried mostly with gradual growth of anaemia. Worsening of the general condition of patient, loss of weight, decreasing  of appetite and waiver of meat are inherent in this pathology.

The gastric bleeding can be related to the diseases of the cardio­ vascular system (atherosclerosis, hypertensive disease), This is mainly seen in the older people.

Other diseases to be differenciated from ulcer bleeding are: the Mallory-Weiss syndrome, benign tumours of stomach and duodenum (more frequent leiomyoma), haemorrhagic gastritis, acute (stress) erosive defects of stomach, arteriovenous fistula of mucosa.

Diagnosis program

1. Anamnesis and physical examination.

2. Digital examination of rectum.

3. FGDS.

4. Laboratory studies.

5. Other necessary instrumental examinations.

Laboratory studies

CBC is necessary to assess the level of blood loss. Where possible, having the patient’s previous results is useful to gauge the level of blood loss. CBC should be checked frequently (4–6 h.) during the first day.

Basic metabolic profile (BMP): The BMP is useful to evaluate for renal comorbidity; however, blood in the upper intestine can elevate the BUN level as well.

Measurement of coagulation parameters is necessary to assess for continued bleeding. Abnormalities should be corrected rapidly.

Prothrombin time/activated partial thromboplastin time.

Liver profile. The liver profile can identify hepatic comorbidity and suggest underlying liver disease.

Calcium level. A calcium level is useful to identify the patient with hyperparathyroidism as well as to monitor calcium in patients receiving multiple transfusions of citrated blood.

Gastrin level. A gastrin level can identify the rare patient with gastrinoma as the cause of peptic ulcer bleeding and multiple ulcers.

Imaging studies

Chest and abdominal radiographs should be ordered to exclude aspiration pneumonia, effusion, and esophageal perforation; abdominal scout and upright films should be ordered to exclude perforated organs and ileus.

Barium contrast studies are not usually helpful and can make endoscopic procedures more difficult (i.e., white barium obscuring the view) and dangerous (i.e., risk of aspiration).

CT scan and ultrasonography may be indicated to evaluate liver disease with cirrhosis, cholecystitis with haemorrhage, pancreatitis with pseudocyst and haemorrhage, aortoenteric fistula, and other unusual causes of upper gastrointestinal haemorrhage.

Nuclear medicine scans may be useful to determine the region of active haemorrhage.

Angiography may be useful if bleeding persists, and endoscopy fails to identify a bleeding site. As salvage therapy, embolization of the bleeding vessel can be as successful as emergent surgery in patients who have failed the second attempt of endoscopic therapy.

Procedures

Nasogastric lavage. This procedure may confirm recent bleeding (coffee ground appearance), possible active bleeding (red blood in the aspirate that does not clear), or a lack of blood in the stomach (active bleeding less likely but does not exclude an upper gastrointestinal lesion).

A nasogastric tube is an important diagnostic tool, and tube placement can reduce the patient’s need to vomit. Placement for diagnostic purposes is not contraindicated in patients with possible esophageal varices.

The characteristics of the nasogastric lavage fluid (e.g., red, coffee grounds, clear) and the stool (e.g., red, black, brown) can indicate the severity of the haemorrhage. Red blood with red stool is associated with an increased mortality rate from more active bleeding compared with negative aspirate findings with brown stool.

 

Policy and choice of treatment method

The main tasks in treatment of patients with acute peptic ulcer haemorrhage are:

1. Arrest of bleeding.

2. Removal of bleeding consequences (correction of blood volume circulation, cardiac, renal, liver disturbances, etc).

3. Antisecretory therapy.

4. Moving off blood from intestine lumen.

5. Immunocorrection.

Arrest of bleeding may be achieved using 3 ways: endoscope, conservative therapy, operation.

Most patients (85–90%) respond to endoscopic therapy. After fiber-optic endoscopy inspection and visualization of the source of bleeding endoscopy hemostasis has been performed using one of the following ways:  

periulcerous injection of vasoconstrictors and procoagulators;

electrocoagulation;

laser coagulation;

plasma coagulation;

covering over the bleeding ulcer with polymer film;

clipping of vessels.

A combination of therapies has become more common. Injection therapy is applied first to better clarify the bleeding site, especially in the actively bleeding patient; then, heater probe or bipolar probe coagulation is applied. Injection therapy can also be performed prior to endoscopic placement of haemoclips. Injection therapy is useful prior to laser therapy to reduce the heat sink effect of rapidly flowing blood prior to laser coagulation.

The use of argon plasma coagulation for ulcer haemorrhage, however, there are significant theoretical and experimental considerations from animal models about the use of a noncontact monopolar cautery in this situation.

The bipolar probe consists of alternating bands of electrodes producing an electrical field that heats the mucosa and the vessel.

The electrodes are coated with gold to reduce adhesiveness. The probes are stiff to allow adequate pressure to the vessel to appose the walls and thus produce coagulation when the energy is transmitted (heat energy by the heater probe, electrical-field energy by the bipolar probe). Careful technique is required to heat-seal the perforated vessel.

Alternatively, epinephrine (1:10,000, 1:20,000) can be injected in 0.5 mL aliquots around the base of the vessel. This causes coagulation by compression, with perhaps some additive effect of activation of platelet factor 3 or vasoconstriction. Other solutions that have been used for injection are ethanol (more necrosis), hypertonic saline, sterile water, and cyanoacrylate.

Epinephrine injection is often used to reduce the volume of bleeding so that the lesion can be better localized and then treated with a coaptive technique (i.e., heater probe, gold probe). Such combination therapy has become more frequent and has evolved into the standard technique.

Laser therapy is rarely used. To perform laser coagulation, the region near the vessel is first injected with epinephrine to reduce blood flow (reducing the heat-sink effect); then, the laser is applied around the vessel (producing a wall of oedema). Caution must be observed to avoid drilling into the vessel with the laser, causing increased bleeding.

Hemostatic clips have recently become available in the United States. With careful placement of the clip, closing the defect in the vessel is possible. Usually, multiple clips are applied.

Argon plasma coagulation is a technique in which a stream of electrons flows along a stream of argon gas. The coagulation is similar to monopolar cautery with the current flow going from a point of high current density, the point of contact of the gas with the mucosa, to an region of low current density, the conductive pad on the patient’s body. The current flows through the body in an erratic path to the pad. This monopolar cautery technique is similar to the laser technique in that energy is delivered to the vessel for coagulation with apposition of the vessel walls. This technique was not effective for visible vessels larger than 1 mm.

Contraindications to emergency fiber-optic endoscopy include:

severe cardiac and lung decompensation;

acute myocardial infarction;

impaired cardiopulmonary status and bleeding diathesis.

Emergency esophagogastroduodenoscopy may be more difficult or impossible if the patient has had previous oropharyngeal surgery or radiation therapy to the oropharynx.

The presence of Zenker’s diverticulum can make intubation of the esophagus more difficult.

After endoscopy hemostasis conservative therapy has been started.

It must include:

prescription of haemostatics (intravenously aminocapronic acid 5% ~ 200–400 ml, chorus calcium 10% – 10.0 ml, vicasol 1% – 3.0 ml);

increasing  of the volume of circulatory blood (gelatin, reopoliglukine, salt blood substitutes);

preparations of blood (fibrinogen – 2–3 g, cryoprecipitate);

blood substitutes therapy (red corpuscles mass, washed red corpuscles, plasma of blood);

H2-receptor antagonists or proton pump inhibitors;

antacids and adsorbents (almagel, phosphalugel, maalox – for 1–2 dessert-spoons through 1 hour after food intake).

It is important to wash stomach with ice water and use 5% solution of aminocapronic acid 1 tablespoon every 20–30 minutes.

Absolute indications for surgical treatment are:

1) prolonged bleeding;

2) recurrent bleeding;

3) perforated bleeding ulcer.

Relative indications for surgery may be established in patients with high risk of recurrent bleeding: Forrest I or II attached to “gigantic” (more than 20 mm in diameter) ulcers, combination of bleeding with stenosis and penetration.

It’s better to perform surgery in the patient at high risk of recurrent bleeding during 24–48 hours after removal of consequences of acute bleeding.

Angiographic embolization is an option in the patient at high risk for surgical intervention. Angiographic embolization of the gastroduodenal or the left gastric arteries may be effective, but there are dangers involved. A foreign body may slip from the gastroduodenal into the hepatic artery and lead to hepatic necrosis; one in the left gastric artery may lead to necrosis of the upper portion of the stomach.

Operations for massively bleeding duodenal ulcers

The site of bleeding must be determined. If the source is the gastroduodenal artery, it must be ligated as the first step. This procedure involves suture of the artery, either above the duodenum as it emerges from the hepatic artery or within the duodenal lumen, suture of the caudal portion of the artery within the duodenum or of the two major branches; the superior pancreatoduodenal and the right gastroepiploic; and of the transverse pancreatic artery. Heavy, non-absorbable sutures are used. In other instances the duodenum may be boggy and bleeding from multiple regions; in such instances it may be impossible to identify vessels to ligate.

As soon as bleeding has been controlled, a definitive operation can be carried out. We believe that ulcer excision and pyloroduodenoplasty with/without selective vagotomy is best. A major determinant in the selection is the experience of the surgeon. If vagotomy wasn’t performed, H2-receptor antagonists or proton pump inhibitors has been prescribed for prevention of ulcer recurrence and it’s complications.

Partial gastrectomy (the usual procedure involves resection of the distal two-thirds of the stomach) is more difficult, but gives slightly better control of bleeding because it removes regions of gastritis and duodenitis that are potential sources of postoperative bleeding.

Operations for bleeding gastric ulcers

Gastric resection is preferred for bleeding gastric ulcers. A truncal vagotomy may be added if the ulcer is in the prepyloric region or if the patient has a history of a duodenal ulcer. Either a Billroth I or II anastomosis can be made.

In some patients who have high operative risks, a local excision of the ulcer may be performed. However, the chances of recurrence within a year approach nearly 50%. Total gastrectomy cannot be determined for.