Although studies in the 1960s and 1970s demonstrated acute erosions of the gastric mucosa in as many

as 60% to 100% of critically ill patients, the incidence has markedly decreased over the past four

decades. Factors postulated to have been important in this phenomenon include (1) the widespread use

of prophylactic gastric alkalinization; (2) improvements in the ability to detect and treat sepsis; (3)

improvements in the ability to monitor and correct hemodynamic instability; and (4) the ability to

provide adequate nutritional support of critically ill patients.

In general, stress gastritis is characterized by the appearance of multiple superficial gastric ulcerations

within 12 to 14 hours of an acute injury. These lesions, initially localized to the fundus and body of the

stomach, later involve the entire gastric surface. Patients at greatest risk include those with sepsis,

major burns, severe trauma, and critically ill patients with a coagulopathy and respiratory

insufficiency.130 In this setting, the disease appears to represent the gastric component of the multiorgan

failure syndrome.

The pathogenesis of this disease is discussed in detail in Chapter 45. The primary defect is in the

protective processes that maintain the integrity of the gastric mucosal barrier. Although some gastric

acid secretion is required for the development of stress gastritis, it is clear that the hypersecretion of

acid is not the cause of mucosal injury. Altered gastric mucosal blood flow and impaired clearance of

hydrogen ions from the mucosa appear to be of particular importance; therefore, the best method of

prevention of stress gastritis is to prevent gastric ischemia and acid injury. Stress gastritis should be

differentiated from the deep, often solitary ulcerations occurring in patients with severe central nervous

system lesions (Cushing ulcers).

Generally hemorrhage is the only symptom that patients with stress gastritis experience. Overt

bleeding is often heralded by the appearance of flecks of blood in the gastric aspirate. The superficial

nature of the lesions makes perforation unlikely.

Prophylactic therapy is directed toward preventing hemorrhage, primarily by neutralizing gastric

acid, augmenting mucosal defenses, and removing or preventing physiologic stress. The gastric pH

should be maintained between 3.5 and 4.5.131 Antacids, H2

-receptor antagonists, PPIs, and sucralfate

have all been used to prevent stress gastritis. Alkalinization of the gastric contents is associated with

oral and fecal flora colonization of the stomach and has raised concerns about an increased risk of

nosocomial pneumonia. This concern prompted the use of sucralfate as a preferred prophylactic agent

for some time instead of antacids or cimetidine.132 However, a prospective, randomized trial of 1,200

critically ill patients receiving either ranitidine or sucralfate for stress ulcer prophylaxis found that those

patients receiving ranitidine had a lower bleeding rate (1.7%) than the sucralfate group (3.8%) but

there was no difference in mortality or incidence of ventilator-assisted pneumonia.133 Since that time,

studies have shown PPIs to be a safe and effective method of stress prophylaxis, but the number of

studies with high-quality data is still lacking.

The success of these prophylactic measures has led to a dearth of recent experience in managing

patients bleeding from stress gastritis. Based on early reports, attention to blood replacement,

intravascular volume restoration, and correction of coagulation defects are associated with the cessation

of hemorrhage in nearly 80% of cases and as such are the principal means of initial treatment. A variety

of nonoperative techniques have been employed with variable success in arresting hemorrhage from

stress gastritis including endoscopic and embolization techniques and the selective catheterization of the

left gastric artery with continuous infusion of vasopressin.134

Based on these same early experiences, very few patients bleeding from erosive gastritis require

operative intervention to arrest hemorrhage. A variety of surgical treatment options have been reported

including vagotomy and pyloroplasty with oversewing of bleeding sites, vagotomy and

hemigastrectomy, total gastrectomy, and gastric devascularization. The dilemma facing the surgeon is

that these critically ill patients poorly tolerate extensive procedures, yet lesser operations often fail to

control hemorrhage. Regardless of the operation performed, mortality risk depends on the underlying

illness, particularly in the presence of multiple organ failure. Mortality rates between 30% and 60% are

commonly quoted, with as many as one-fourth of the deaths resulting from continued hemorrhage.

Rebleeding rates ranging from 25% to 61% have been reported. The combination of vagotomy,

hemigastrectomy, and oversewing of bleeding points has been touted as more successful in these

patients; however, rebleeding rates of 11% to 44% and operative mortality rates ranging from 33% to

63% have been associated with this procedure.135 More extensive operations, such as near total

gastrectomy or total gastrectomy are associated with significant mortality although they successfully

stop hemorrhage.

Gastroesophageal Varices

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Cirrhosis is a leading cause of death in the United States and variceal hemorrhage is a common mode of

death for these patients. About 30% of people with cirrhosis develop gastroesophageal varices; of these

individuals, about 30% bleed as a result of the varices, usually within 1 to 2 years of diagnosis.

Gastroesophageal varices are a significant cause of UGI hemorrhage, accounting for about 20% of such

cases. Patients with bleeding gastroesophageal varices tend to have much higher rebleeding rates,

transfusion requirements, lengths of hospitalization, and risk of death than do patients bleeding from

nonvariceal causes.120,136

Although the basic tenets of resuscitation for massive variceal hemorrhage are similar to those for any

cause of massive bleeding, intravenous volume resuscitation should be particularly judicious. The

hyperaldosteronemic state of cirrhosis promotes sodium and water retention with aggravation of ascites

and peripheral edema. Accurate blood replacement is imperative since overtransfusion may worsen

portal hypertension and exacerbate hemorrhage. Invasive cardiac monitoring with Swan–Ganz

catheterization may be particularly useful for guiding volume replacement. Coagulation deficits should

be aggressively corrected by administering fresh frozen plasma. Thrombocytopenia, secondary to

hypersplenism or dilution, should be treated promptly with pooled platelet transfusions. Sedatives are

best avoided or used sparingly because cirrhosis impairs the liver’s ability to metabolize many of these

drugs. Adequate prophylaxis for delirium tremens should be administered to alcoholics.

As with other sources of UGI hemorrhage, early endoscopy is imperative for successful diagnosis and

therapy.137 The identification of varices alone is not adequate to incriminate them as the source of the

hemorrhage since up to half of patients with cirrhosis bleed from a source other than varices.

Furthermore, endoscopy may identify factors associated with a heightened risk of variceal hemorrhage

such as the size and number of varices and the presence of red, blue, or other colored spots on the varix.

The presence of gastric and duodenal varices and portal hypertensive changes in the gastric mucosa

(portal gastropathy) will influence therapeutic decisions and prognosis.

Although vasopressin has commonly been used in the management of variceal hemorrhage, its use has

been limited due to the potent vasoconstrictive properties causing cardiac and peripheral ischemia,

arrhythmias, hypertension, and bowel ischemia. More recent reports suggest the superiority of

somatostatin or its synthetic analog, octreotide. It is thought that octreotide causes splanchnic arteriolar

vasoconstriction and reduces variceal and azygous vein flow with limited direct effects on portal

pressure.138 Meta-analyses have shown that the infusion of somatostatin is more effective and safer than

vasopressin in the pharmacologic control of variceal hemorrhage.139,140 Other studies have shown that

somatostatin or octreotide can improve the results of sclerotherapy or endoscopic variceal

ligation.141,142 Although neither somatostatin nor vasopressin plus nitroglycerin definitively treat the

bleeding esophageal varices, these modalities may provide initial control of hemorrhage, reducing

transfusion requirements and providing time for resuscitation before definitive treatment.

Another temporizing method used for massively bleeding patients is balloon tamponade using a

Sengstaken–Blakemore tube or a Minnesota tube. These devices consist of a gastric tube with

esophageal and gastric balloons. In the case of a Minnesota tube, a proximal esophageal lumen allows

for the aspiration of swallowed secretions. Inflation of the gastric (and if required esophageal) balloons

tamponade the bleeding varices, controlling hemorrhage in more than 80% of cases. Hemorrhage recurs

in 25% to 50% of patients upon deflation of the balloons, thus limiting this technique to a temporizing

role.143 The greatest value of these tubes is for arresting massive hemorrhage that has been

unresponsive to other measures, allowing time for resuscitation and angiographic definition of the

portal system before definitive treatment.

When used inappropriately, these tubes can be associated with significant morbidity and mortality.

Complications occur in 4% to 9% of patients with the most frequent being aspiration pneumonitis.

Measures to prevent pulmonary complications include endotracheal intubation before tube insertion and

the placement of an esophageal tube to remove swallowed salivary secretions. Other significant

complications include esophageal rupture or necrosis and airway occlusion during the attempted

removal of an incompletely deflated gastric balloon. Because of the availability of endoscopy, these

tubes are rarely used today.

8 Endoscopic sclerotherapy, endoscopic clipping or endoscopic variceal ligation (banding) have

become the most widely used modalities for the initial definitive control of bleeding esophageal varices.

Several studies have confirmed that these techniques arrest acute variceal hemorrhage in 90% to 95% of

patients. In general, a patient bleeding from esophageal varices should undergo urgent pharmacologic

therapy and banding of the varices at the time of the first emergency endoscopy. Sclerotherapy can be

used if ligation is technically difficult.137 A single endoscopic treatment controls variceal bleeding in

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