Peptic ulcer disease (gastric and duodenal ulcers), which results from the breakdown of the gastromucosal lining, is the leading cause of upper gastrointestinal hemorrhage, accounting for approximately 21% of cases.4 Normally, protection of the gastric mucosa from the digestive effects of gastric secretions is accomplished in several ways. First, the gastroduodenal mucosa is coated by a glycoprotein mucous barrier that protects the surface of the epithelium from hydrogen ions and other noxious substances present in the gut lumen.^6,7 Adequate gastric mucosal blood flow is necessary to maintain this mucosal barrier function. Second, gastroduodenal epithelial cells are protected structurally against damage from acid and pepsin because they are connected by tight junctions that help prevent acid penetration. Third, prostaglandins and nitric oxide protect the mucosal barrier by stimulating mucus and bicarbonate secretion and inhibiting the secretion of acid.⁷

Peptic ulceration occurs when these protective mechanisms cease to function, allowing gastroduodenal mucosal breakdown. After the mucosal lining is penetrated, gastric secretions autodigest the layers of the stomach or duodenum, leading to injury of the mucosal and submucosal layers. This results in damaged blood vessels and subsequent hemorrhage. The two main causes of disruption of gastroduodenal mucosal resistance are nonsteroidal antiinflammatory drugs and the bacterial action of Helicobacter pylori.^4,8,9

Stress-related mucosal disease (SRMD) is an acute erosive gastritis that covers both types of mucosal lesions that are often found in the critically ill patient: stress-related injury and discrete stress ulcers.10,11 These abnormalities develop within hours of admission.¹⁰ They range from superficial mucosal erosions to deep focal lesions and usually affect the upper gastrointestinal tract.¹⁰ SRMD occurs by means of the same pathophysiological mechanisms as peptic ulcer disease, but the main cause of disruption of gastric mucosal resistance is increased acid production and decreased mucosal blood flow, resulting in ischemia and degeneration of the mucosal lining.^10,11 Patients at risk include those in situations of high physiological stress, such as occur with mechanical ventilation, extensive burns, severe trauma, major surgery, shock, sepsis, coagulopathy, or acute neurological disease.^10,11 Gastroduodenal lesions are estimated to occur in 75% to 100% of ICU patients within 24 hours of admission.¹⁰ SRMD is a leading cause of upper gastrointestinal hemorrhage, accounting for approximately 15% of cases.¹¹

Esophagogastric varices are engorged and distended blood vessels of the esophagus and proximal stomach that develop as a result of portal hypertension caused by hepatic cirrhosis, a chronic disease of the liver that results in damage to the liver sinusoids (Figure 22-1). Without adequate sinusoid function, resistance to portal blood flow is increased, and pressures within the liver are elevated. This leads to increased portal venous pressure (portal hypertension), causing collateral circulation to divert portal blood from areas of high pressure within the liver to adjacent areas of low pressure outside the liver, such as into the veins of the esophagus, the spleen, the intestines, and the stomach. The tiny, thin-walled vessels of the esophagus and proximal stomach that receive this diverted blood lack sturdy mucosal protection. The vessels become engorged and dilated, forming esophagogastric varices that are vulnerable to damage from gastric secretions and that may result in subsequent rupture and massive hemorrhage.¹² The risk of variceal bleeding increases with disease severity and variceal size, but overall, bleeding occurs in up to 30% of patients with medium or large varices, and only 50% of patients stop bleeding spontaneously.^12,13

The patient who is vomiting blood is usually bleeding from a source above the duodenojejunal junction; reverse peristalsis is seldom sufficient to cause hematemesis if the bleeding point is below this area. The hematemesis may be bright red or look like coffee grounds, depending on the amount of gastric contents at the time of bleeding and the length of time the blood has been in contact with gastric secretions. Gastric acid converts bright red hemoglobin to brown hematin, accounting for the coffee grounds appearance of the emesis. Bright red emesis results from profuse bleeding with little contact with gastric secretions.1

The presence of blood in the gastrointestinal tract results in increased peristalsis and diarrhea. Hematochezia (bright red stool) occurs from massive lower gastrointestinal hemorrhage and, if rapid enough, upper gastrointestinal hemorrhage. Melena (black, tarry, or dark red stool) occurs from digestion of blood from an upper gastrointestinal hemorrhage and may take several days to clear after the bleeding has stopped.2,4

Laboratory tests can help to determine the extent of bleeding, although the patient’s hemoglobin level and hematocrit are poor indicators of the severity of blood loss if the bleeding is acute. As whole blood is lost, plasma and red blood cells are lost in the same proportion; if the patient’s hematocrit is 45% before a bleeding episode, it will be 45% several hours later.7 It may take as long as 72 hours for the redistribution of plasma from the extravascular space to the intravascular space to occur and cause the patient’s hemoglobin level and hematocrit value to decrease.¹⁴

To isolate and treat the source of bleeding, an urgent fiberoptic endoscopy is usually undertaken. If performed within 12 hours of the bleeding event, endoscopy therapy has a 90% effectiveness rate in achieving hemostasis and reducing mortality.1,2 Before endoscopy, the patient must be hemodynamically stabilized.¹⁵ Tagged red blood cell scanning or angiography, or both, may be done to assist with localizing and treating a bleeding lesion in the gastrointestinal tract when it is impossible to clearly view the gastrointestinal tract because of continued active bleeding.^1,5

The initial treatment priority is the restoration of adequate circulating blood volume to treat or prevent shock. This is accomplished with the administration of intravenous infusions of crystalloids, blood, and blood products.13,15,16 Hemodynamic monitoring can help to guide fluid replacement therapy,⁸ particularly in patients at risk for cardiac failure. Supplemental oxygen therapy is initiated to increase oxygen delivery and improve tissue perfusion.^2,5 Intubation may be necessary in the patient at risk for aspiration or to facilitate gastric lavage.¹⁵ A large nasogastric tube may be inserted to confirm the diagnosis of active bleeding and to prepare the esophagus, stomach, and proximal duodenum for endoscopic evaluation.^1,2 A urinary drainage catheter should be inserted to monitor urine output.¹⁴

Measures to facilitate volume replacement include obtaining intravenous access and administering prescribed fluids and blood products. Two large-diameter peripheral intravenous catheters should be inserted to facilitate the rapid administration of prescribed fluids.13

One measure to control active bleeding is gastric lavage. It is used to decrease gastric mucosal blood flow and evacuate blood from the stomach. Gastric lavage is performed by inserting a large-bore nasogastric tube into the stomach and irrigating it with normal saline or water until the returned solution is clear. It is important to keep accurate records of the amount of fluid instilled and aspirated to ascertain the true amount of bleeding.1 Historically, iced saline was favored as a lavage irrigant. Research has shown, however, that low-temperature fluids shift the oxyhemoglobin dissociation curve to the left, decrease oxygen delivery to vital organs, and prolong bleeding time and prothrombin time. Iced saline also may further aggravate bleeding; therefore room-temperature water or saline is the preferred irrigant for use in gastric lavage.²¹

The patient should be continuously observed for signs of gastric perforation. Although a rare complication, gastric perforation constitutes a surgical emergency. Signs and symptoms include sudden, severe, generalized abdominal pain with significant rebound tenderness and rigidity. Perforation should be suspected when fever, leukocytosis, and tachycardia persist despite adequate volume replacement.9

The results of physical assessment usually reveal hypoactive bowel sounds and abdominal tenderness, guarding, distention, and tympany. Findings that may indicate pancreatic hemorrhage include Grey Turner’s sign (gray-blue discoloration of the flanks) and Cullen’s sign (discoloration of the umbilical region); however, they are rare and usually seen several days into the illness.22 A palpable abdominal mass indicates the presence of a pseudocyst or abscess.²⁶

Assessment of laboratory data usually demonstrates elevated levels of serum amylase and lipase. Serum lipase is more pancreas-specific than amylase and a more accurate marker for acute pancreatitis. Amylase is present in other body tissues, and other disorders (e.g., intraabdominal emergencies, renal insufficiency, salivary gland trauma, liver disease) may contribute to an elevated level. Unlike other serum enzymes, however, amylase is excreted in urine, and this clearance increases with acute pancreatitis. Measurement of urinary versus serum amylase should be considered in light of the patient’s creatinine clearance. The serum amylase level may be elevated for only 3 to 5 days; if the patient delays seeking treatment, a normal level (false-negative result) may be detected. Leukocytosis, hypocalcemia, hyperglycemia, hyperbilirubinemia, and hypoalbuminemia may also be present (Table 22-2).^8,22,23

An abdominal ultrasound scan is obtained as part of the diagnostic evaluation to determine the presence of biliary stones. A contrast-enhanced computed tomography (CT) scan is considered the gold standard for diagnosing pancreatitis and for ascertaining the overall degree of pancreatic inflammation and necrosis.22,23

Because pancreatitis if often associated with massive fluid shifts, intravenous crystalloids and colloids are administered immediately to prevent hypovolemic shock and maintain hemodynamic stability. In severe forms of acute pancreatitis, a pulmonary artery catheter may be used to guide ongoing fluid management.25 Electrolytes are monitored closely, and abnormalities such as hypocalcemia, hypokalemia, and hypomagnesemia are corrected.^22,25 If hyperglycemia develops, exogenous insulin may be required.²⁵

Over the past 3 decades, nutritional support has shifted. Previously, conventional nutritional management was to place the patient on a no oral intake (NPO) regimen and institute intravenous hydration. The rationale was to rest the inflamed pancreas and prevent enzyme release. Oral feeding was initiated only when the attack had subsided and enzymes had normalized. Total parenteral nutrition (TPN) was started for patients anticipated to have oral feedings held for more than 5 days. Randomized clinical trials have demonstrated that enteral feeding (gastric or jejunal) is safe and cost-effective and that it is associated with fewer septic and metabolic complications than other methods.27,28 Enteral feeding enhances immune modulation and maintenance of the intestinal barrier, and it avoids complications associated with parental nutrition.^27–29 Early initiation of enteral feeding is preferred over TPN.^27–29 However, TPN still has a role for the critically ill patient with acute pancreatitis who does not tolerate enteral feeding or when nutritional goals are not reached within 2 days.^23,27 In the past, nasogastric suction was also recommended, but this intervention has not been shown to be of benefit and should be instituted only if the patient has persistent vomiting, obstruction, or gastric distention.²²

Acute pancreatitis can affect every organ system, and recognition and treatment of systemic complications are crucial to management of the patient (Box 22-5). The most serious complications are hypovolemic shock, acute lung injury (ALI), acute renal failure (ARF), and gastrointestinal hemorrhage. Hypovolemic shock is the result of relative hypovolemia resulting from third spacing of intravascular volume and vasodilation caused by the release of inflammatory immune mediators. These mediators also contribute to the development of ALI and ARF. Other possible pulmonary complications include pleural effusions, atelectasis, and pneumonia.

Local complications include the development of infected pancreatic necrosis and pancreatic pseudocyst.23,27 The necrotic areas of the pancreas can lead to development of a widespread pancreatic infection (infected pancreatic necrosis), which significantly increases the risk of death.²⁷

Prophylactic antibiotics reduce sepsis and mortality and are initiated in patients suspected of having necrotizing pancreatitis.²⁷ After the patient develops infected necrosis, however, surgical débridement is necessary.^23,27 The procedure of choice is a minimally invasive necrosectomy, which entails careful débridement of the necrotic tissue in and around the pancreas. A pancreatic pseudocyst is a collection of pancreatic fluid enclosed by a nonepithelialized wall.²⁶ Cyst formation may result from liquefaction of a pancreatic fluid collection or from direct obstruction in the main pancreatic duct.²⁴ A pancreatic pseudocyst may (1) resolve spontaneously; (2) rupture, resulting in peritonitis; (3) erode a major blood vessel, resulting in hemorrhage; (4) become infected, resulting in abscess; or (5) invade surrounding structures, resulting in obstruction.²⁴ Treatment involves drainage of the pseudocyst surgically,³⁰ endoscopically, or percutaneously.^23,27

Pain management is a major priority in acute pancreatitis. Administration of analgesics to achieve pain relief is essential. For years, meperidine (Demerol) was considered to be the preferred agent in the patient with acute pancreatitis because morphine produced spasms at the sphincter of Oddi. However, studies have demonstrated that all opioids have a spasmogenic effect on the sphincter of Oddi. There is no evidence to indicate that morphine is contraindicated for use in acute pancreatitis, and it may provide more effective analgesia with fewer side effects than meperidine.22,27 Relaxation techniques and positioning the patient in the knee-chest position can also assist in pain control.

The patient must be routinely monitored for signs of local or systemic complications (see Box 22-5). Intensive monitoring of each of the organ systems is imperative, because organ failure is a major indicator of the severity of the disease.³¹ The patient must be closely monitored for signs and symptoms of pancreatic infection, which include increased abdominal pain and tenderness, fever, and increased white blood cell count (Box 22-6).²²

Early in the patient’s hospital stay, the patient and family should be taught about acute pancreatitis and its causes and treatment. As the patient moves toward discharge, teaching should focus on the interventions necessary for preventing the recurrence of the precipitating disorder. If there is sustained, permanent damage to the pancreas, the patient will require teaching specific to diet modification and supplemental pancreatic enzymes. Diabetes education may also be necessary. If an alcohol abuser, the patient should be encouraged to stop drinking and be referred to an alcohol cessation program (Patient Education Box on Acute Pancreatitis).25 Collaborative management of the patient is outlined in the Box on Collaborative Management of Acute Pancreatitis.