Gastrointestinal Disorders and Therapeutic Management

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Gastrointestinal Disorders and Therapeutic Management

Sheryl E. Leary

Objectives

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Be sure to check out the bonus material, including free self-assessment exercises, on the Evolve web site at evolve.elsevier.com/Urden/priorities.

Understanding the pathology of a disease, the areas of assessment on which to focus, and the usual medical management allows the critical care nurse to accurately anticipate and plan nursing interventions. This chapter focuses on gastrointestinal disorders commonly seen in the critical care environment.

Acute Gastrointestinal Hemorrhage

Gastrointestinal hemorrhage is a potentially life-threatening emergency that remains a common complication of critical illness1 and results in 400,000 hospital admissions yearly.2 Despite advances in medical knowledge and nursing care, the mortality rate for patients with acute gastrointestinal bleeding remains at 10%.1,3

Etiology

Gastrointestinal hemorrhage occurs from bleeding in the upper or lower gastrointestinal tract. The ligament of Treitz is the anatomic division used to differentiate between the two areas. Bleeding proximal to the ligament is considered to be upper gastrointestinal in origin, and bleeding distal to the ligament is considered to be lower gastrointestinal in origin.1,4 The various causes of acute gastrointestinal hemorrhage are listed in Box 22-1.4,5 Only the three main causes of gastrointestinal hemorrhage commonly seen in the intensive care unit (ICU) are discussed further.

Peptic Ulcer Disease

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

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

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

Pathophysiology

Gastrointestinal hemorrhage is a life-threatening disorder that is characterized by acute, massive bleeding. Regardless of the cause, acute gastrointestinal hemorrhage results in hypovolemic shock, initiation of the shock response, and development of multiple organ dysfunction syndrome if left untreated (Concept Map on Acute Gastrointestinal Hemorrhage).7 However, the most common cause of death in cases of gastrointestinal hemorrhage is exacerbation of the underlying disease, not intractable hypovolemic shock.

Assessment and Diagnosis

The initial clinical presentation of the patient with acute gastrointestinal hemorrhage is that of a patient in hypovolemic shock, and the clinical presentation depends on the amount of blood lost (Table 22-1).7 Hematemesis (bright red or brown, coffee grounds emesis), hematochezia (bright red stools), and melena (black, tarry, or dark red stools) are the hallmarks of gastrointestinal hemorrhage.1,4,5

TABLE 22-1

CLINICAL CLASSIFICATION OF HEMORRHAGE

CLASS BLOOD LOSS (%) CLINICAL SIGNS AND SYMPTOMS
1 ≤15 Pulse rate: normal or <100 beats/min (supine)
Capillary refill <3 sec
Urine output: adequate (30-35 mL/hr)
Orthostatic hypotension
Apprehensive
2 15-30 Pulse rate: increased (>100 beats/min)
Capillary refill: sluggish
Pulse pressure: decreased
Blood pressure: normal (supine)
Tachypnea
Urine output: low (25-30 mL/hr)
3 30-40 Pulse rate: 120+ beats/min (supine)
Hypotension
Skin: cool, pale
Confused
Hyperventilating
Urine output: low (5-15 mL/hr)
4 ≥40 Profoundly hypotensive
Pulse rate: 140+ beats/min
Confused, lethargic
Urine output minimal

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From Klein DG: Physiologic response to traumatic shock, AACN Clin Issues Crit Care Nurs 1(3):505, 1990.

Hematemesis

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

Hematochezia and Melena

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 Studies

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

Diagnostic Procedures

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

Medical Management

To reduce mortality related to gastrointestinal hemorrhage, patients at risk should be identified early, and interventions should be implemented to reduce gastric acidity and support the gastric mucosal defense mechanisms. Management of the patient at risk for gastrointestinal hemorrhage should include prophylactic administration of pharmacological agents for gastric acid neutralization. These agents include antacids, histamine-2 (H2) antagonists, cytoprotective agents, and proton-pump inhibitors (PPIs).10,11

Priorities in the medical management of the patient with gastrointestinal hemorrhage include airway protection, fluid resuscitation to achieve hemodynamic stability, correction of comorbid conditions (e.g., coagulopathy), therapeutic procedures to control or stop bleeding, and diagnostic procedures to determine the exact cause of the bleeding.1,2,15

Stabilization

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

Controlling the Bleeding

Interventions to control bleeding are the second priority for the patient with gastrointestinal hemorrhage.

Peptic Ulcer Disease

In the patient with gastrointestinal hemorrhage related to peptic ulcer disease, bleeding hemostasis may be accomplished by endoscopic injection therapy in conjunction with thermal or hemostatic clips.2,17 Endoscopic thermal therapy uses heat to cauterize the bleeding vessel, and endoscopic injection therapy uses a variety of agents such as hypertonic saline, epinephrine, ethanol, and sclerosants to induce localized vasoconstriction of the bleeding vessel.1,2,17 Intraarterial infusion of vasopressin into the gastric artery or intraarterial injection of an embolizing agent (e.g., Gelfoam pledgets, polyvinyl alcohol particles, coils) can be performed during arteriography to control bleeding after the site has been identified.2

Stress-Related Mucosal Disease

In the patient with gastrointestinal hemorrhage caused by SRMD, bleeding hemostasis may be accomplished by intraarterial infusion of vasopressin and intraarterial embolization. Endoscopic therapies provide minimal benefit because of the diffuse nature of the disease.15

Esophagogastric Varices

In acute variceal hemorrhage, control of bleeding may be initially accomplished through the use of pharmacological agents and endoscopic variceal ligation.13 Intravenous vasopressin, somatostatin, and octreotide can reduce portal venous pressure and slow variceal hemorrhaging by constricting the splanchnic arteriolar bed.18 Endoscopic variceal ligation is the preferred endoscopic therapy for controlling acute gastrointestinal bleeding related to varices. Bands are placed around the varices to create an obstruction to stop the bleeding.13

If these initial therapies fail, transjugular intrahepatic portosystemic shunting (TIPS) or esophagogastric balloon tamponade may be necessary. In a TIPS procedure, a channel between the systemic and portal venous systems is created to redirect portal blood, thereby reducing portal hypertension and decompressing the varices to control bleeding (Figure 22-2).1,13 Balloon tamponade tubes (Sengstaken-Blakemore, Linton, and Minnesota tubes) stop hemorrhaging by applying direct pressure against bleeding vessels while decompressing the stomach.19 This therapy is rarely needed anymore given the success rate of the other therapies.

Surgical Intervention

The patient who remains hemodynamically unstable despite volume replacement may need urgent surgery.

Peptic Ulcer Disease

The operative procedure of choice to control bleeding from peptic ulcer disease is a vagotomy and pyloroplasty. During this procedure, the vagus nerve to the stomach is severed, eliminating the autonomic stimulus to the gastric cells and reducing hydrochloric acid production. Because the vagus nerve also stimulates motility, a pyloroplasty is performed to provide for gastric emptying.9

Stress-Related Mucosal Disease

Several operative procedures can be used to control bleeding from SRMD. A total gastrectomy is performed when bleeding is generalized. The ulcers are oversewn when bleeding is localized.20 Total gastrectomy involves the complete removal of the stomach with anastomosis of the esophagus to the jejunum. During an oversew of the ulcers, the bleeding vessel is ligated, and the ulcer crater is closed.16,20

Esophagogastric Varices

Operative procedures to control bleeding gastroesophageal varices include portacaval shunt, mesocaval shunt, and splenorenal shunt (Figure 22-3).20 These shunt procedures are also referred to as decompression procedures, because they result in the diversion of portal blood flow away from the liver and decompression of the portal system. The portacaval shunt procedure has two variations. An end-to-side portacaval shunt procedure involves the ligation of the hepatic end of the portal vein with subsequent anastomosis to the vena cava. During a side-to-side portacaval shunt procedure, the side of the portal vein is anastomosed to the side of the vena cava. A mesocaval shunt procedure involves the insertion of a graft between the superior mesenteric artery and the vena cava. During a distal splenorenal shunt procedure, the splenic vein is detached from the portal vein and anastomosed to the left renal vein.20

Nursing Management

All critically ill patients should be considered at risk for stress ulcers and therefore gastrointestinal hemorrhage. Patients at risk also should be assessed for the presence of bright red or coffee grounds emesis; bloody nasogastric aspirate; and bright red, black, or dark red stools. Any signs of bleeding should be promptly reported to the physician.

Nursing management of a patient experiencing acute gastrointestinal hemorrhage incorporates a variety of nursing diagnoses (Nursing Diagnosis Priorities Box on Acute Gastrointestinal Hemorrhage). Nursing priorities are directed toward (1) administering volume replacement, (2) controlling the bleeding, (3) providing comfort and emotional support, (4) maintaining surveillance for complications, and (5) educating the patient and family.

Administering Volume Replacement

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

Controlling the Bleeding

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

Maintaining Surveillance for Complications

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

Educating the Patient and Family

Early in the hospital stay, the patient and family should be taught about acute gastrointestinal hemorrhage and its causes and treatments. As the patient moves toward discharge, teaching should focus on the interventions necessary for preventing the recurrence of the precipitating disorder. 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 Gastrointestinal Hemorrhage). Collaborative management of the patient is outlined in the Box on Collaborative Management of Acute Gastrointestinal Hemorrhage.

Acute Pancreatitis

Acute pancreatitis is an inflammation of the pancreas that produces exocrine and endocrine dysfunction that may also involve surrounding tissues and/or remote organ systems. The clinical course can range from a mild, self-limiting disease to a systemic process characterized by organ failure, sepsis, and death. In approximately 80% of patients, it takes the milder form of edematous interstitial pancreatitis, whereas the other 20% develop severe acute necrotizing pancreatitis.22 Reported mortality rates for acute pancreatitis range from 2% to 15% overall and from 20% to 50% for patients with severe disease.22,23 Several prognostic scoring systems have been developed to predict the severity of acute pancreatitis. One of the most commonly used is Ranson’s criteria (Box 22-2). If the patient has 0 to 2 factors present, the predicted mortality rate is 2%; with 3 to 4 factors, the rate is 15%; with 5 to 6 factors, the rate is 40%; and with 7 to 8 factors, predicted mortality rate is 100%.22,24

Etiology

The two most common causes of acute pancreatitis are gallstones and alcoholism. Together, they account for approximately 80% of cases. Less common causes are quite diverse and include surgical trauma, hypercalcemia, various toxins, ischemia, infections, and the use of certain drugs (Box 22-3). In 10% to 20% of patients with acute pancreatitis, no etiologic factor can be determined.23

Pathophysiology

In acute pancreatitis, the normally inactive digestive enzymes become prematurely activated within the pancreas itself, leading to autodigestion of pancreatic tissue. The enzymes become activated through various mechanisms, including obstruction of or damage to the pancreatic duct system, alterations in the secretory processes of the acinar cells, infection, ischemia, and other unknown factors.8,22

Trypsin is the enzyme that becomes activated first. It initiates the autodigestion process by triggering the secretion of proteolytic enzymes such as kallikrein, chymotrypsin, elastase, phospholipase A, and lipase. Release of kallikrein and chymotrypsin results in increased capillary membrane permeability, leading to leakage of fluid into the interstitium and the development of edema and relative hypovolemia. Elastase is the most harmful enzyme in terms of direct cell damage. It dissolves the elastic fibers of blood vessels and ducts, leading to hemorrhage. Phospholipase A, in the presence of bile, destroys the phospholipids of cell membranes, causing severe pancreatic and adipose tissue necrosis. Lipase flows into the damaged tissue and is absorbed into the systemic circulation, resulting in fat necrosis of the pancreas and surrounding tissues.8,22

The extent of injury to the pancreatic cells determines the type of acute pancreatitis that develops. If injury to the pancreatic cells is mild and without necrosis, edematous pancreatitis develops. The acinar cells appear structurally intact, and blood flow is maintained through small capillaries and venules. This form of acute pancreatitis is self-limiting. If injury to the pancreatic cells is severe, acute necrotizing pancreatitis develops.22,23 Cellular destruction in pancreatic injury results in the release of toxic enzymes and inflammatory mediators into the systemic circulation and causes injury to vessels and other organs distant from the pancreas; this may result in systemic inflammatory response syndrome (SIRS), multiorgan failure, and death.22,23 Local tissue injury results in infection, abscess and pseudocyst formation, disruption of the pancreatic duct, and severe hemorrhage with shock.22

Assessment and Diagnosis

The clinical manifestations of acute pancreatitis range from mild to severe and often mimic those of other disorders (Box 22-4). Acute onset of abdominal pain is a hallmark symptom.23 Epigastric to periumbilical pain may vary from mild and tolerable to severe and incapacitating. Many patients report a twisting or knifelike sensation that radiates to the low dorsal region of the back. The patient may obtain some comfort by leaning forward or assuming a semifetal position. Nausea and vomiting are common.23 Other clinical findings include fever, diaphoresis, weakness, tachypnea, hypotension, and tachycardia. Depending on the extent of fluid loss and hemorrhage, the patient may exhibit signs of hypovolemic shock.22,23,25

Box 22-4

Presenting Clinical Manifestations of Acute Pancreatitis

Mild Disease

Severe Disease

From Krumberger JM: Acute pancreatitis, Crit Care Nurs Clin North Am 5(1):185, 1993.

Physical Examination

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

Laboratory Studies

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

TABLE 22-2

LABORATORY TESTS AND DIAGNOSTIC PROCEDURES FOR ACUTE PANCREATITIS

STUDY FINDING IN PANCREATITIS
Laboratory Studies  
Serum amylase Elevated
Serum isoamylase Elevated
Urine amylase Elevated
Serum lipase (if available) Elevated
Serum triglycerides Elevated
Glucose Elevated
Calcium Decreased
Magnesium Decreased
Potassium Decreased
Albumin Decreased or increased
White blood cell count Elevated
Bilirubin May be elevated
Liver enzymes May be elevated
Prothrombin time Prolonged
Arterial blood gases Hypoxemia, metabolic acidosis
Diagnostic Procedures  
Abdominal ultrasonography  
Computed tomography scan  
Magnetic resonance imaging  
Endoscopic retrograde cholangiopancreatography  
Abdominal radiographs (flat plate and upright or decubitus)  
Chest radiographs (posteroanterior and lateral)  

Modified from Krumberger JM: Acute pancreatitis, Crit Care Nurs Clin North Am 5(1):185, 1993.

Diagnostic Procedures

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

Medical Management

Initial management of the patient with severe acute pancreatitis includes ensuring adequate fluid and electrolyte replacement, providing nutritional support, and correcting metabolic alterations.23 Careful monitoring for systemic and local complications is critical.22,24,25

Fluid Management

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

Nutritional Support

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.2729 Early initiation of enteral feeding is preferred over TPN.2729 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

Systemic Complications

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

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

Nursing Management

Nursing management of the patient with pancreatitis incorporates a variety of nursing diagnoses (Nursing Diagnosis Priorities Box on Acute Pancreatitis). Nursing priorities are directed toward (1) providing pain relief and emotional support, (2) maintaining surveillance for complications, and (3) educating the patient and family.

Providing Comfort and Emotional Support

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.

Maintaining Surveillance for Complications

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

Educating the Patient and Family

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.

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