Etiology

GI hemorrhage occurs from bleeding in the upper or lower GI 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 from the upper GI tract, and bleeding distal to the ligament is considered to be from the lower GI tract.1–3 The various causes of acute GI hemorrhage are listed in Box 30-1.⁴ Only the three main causes of GI hemorrhage commonly seen in the critical care unit are discussed further.

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.¹⁹

Hematochezia and Melena

The presence of blood in the GI tract results in increased peristalsis and diarrhea. Hematochezia occurs from massive lower GI hemorrhage and, if rapid enough, upper GI hemorrhage. Melena occurs from digestion of blood from an upper GI hemorrhage and may take several days to clear after the bleeding has stopped.

Laboratory Studies

Laboratory tests can help 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 24 to 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.¹⁹

Diagnostic Procedures

To isolate and treat the source of bleeding, an urgent fiberoptic endoscopy is usually undertaken.²⁰ Before endoscopy, the patient must be hemodynamically stabilized.²¹ Tagged red blood cell scanning, angiography, or both, may be done to assist with localizing and treating a bleeding lesion in the GI tract when it is impossible to clearly view the GI tract because of continued active bleeding.¹⁹

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.²² Hemodynamic monitoring can help guide fluid replacement therapy, particularly in patients at risk for heart failure.⁷ Supplemental oxygen therapy is initiated to increase oxygen delivery and improve tissue perfusion.^7,22 A large nasogastric tube may be inserted to confirm the diagnosis of active bleeding, to facilitate gastric lavage, decrease the risk for aspiration and to prepare the esophagus, stomach, and proximal duodenum for endoscopic evaluation.⁵

Controlling the Bleeding

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

Esophagogastric Varices.

In acute variceal hemorrhage, control of bleeding may be initially accomplished through the use of pharmacologic agents and endoscopic therapies. Intravenous vasopressin, somatostatin, and octreotide can reduce portal venous pressure and slow variceal hemorrhaging by constricting the splanchnic arteriolar bed.¹⁶ Two commonly used endoscopic therapies are endoscopic injection sclerotherapy (EIS) and endoscopic variceal ligation (EVL).²³ EIS controls bleeding by the injection of a sclerosing agent in or around the varices. This creates an inflammatory reaction that induces vasoconstriction and results in the formation of a venous thrombosis. During EVL, bands are placed around the varices to create an obstruction to stop the bleeding.²⁴

If these initial therapies fail, transjugular intrahepatic portosystemic shunting (TIPS) 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 (Fig. 30-3).^23,24

Surgical Intervention

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

Esophagogastric Varices.

If medical treatment is unsuccessful and angiographic interventional TIPS procedure is not available, operative procedures to control bleeding gastroesophageal varices may be undertaken. Though rarely performed, operative interventions focus on some form of shunting (Fig 30-4).²⁵ 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: (1) an end-to-side portacaval shunt procedure, which involves the ligation of the hepatic end of the portal vein with subsequent anastomosis to the vena cava; and (2) a side-to-side portacaval shunt procedure, during which 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.²⁷

Etiology

The two most common causes of acute pancreatitis are gallstone migration and alcoholism.³⁶ Together, they account for approximately 80% of cases.¹⁹ Less common causes are quite diverse and include surgical trauma, hypercalcemia, various toxins, ischemia, infections, and the use of certain medications (Box 30-6). In up to 20% of patients with acute pancreatitis, no etiologic factor can be determined.^19,31

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.7,36

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.7,37

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.32,37 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.^19,36 Local tissue injury results in infection, abscess and pseudocyst formation, disruption of the pancreatic duct, and severe hemorrhage and shock.¹⁹

Assessment and Diagnosis

The clinical manifestations of acute pancreatitis range from mild to severe and often mimic those of other disorders (Box 30-7). Acute onset of abdominal pain, nausea, and vomiting are hallmark symptoms.^19,32,37 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. 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.^19,37

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. Electrolytes are monitored closely, and abnormalities such as hypocalcemia, hypokalemia, and hypomagnesemia are corrected.³⁷ If hyperglycemia develops, exogenous insulin may be required.

Nutritional Support

Over the past three decades, nutritional support has shifted. Previously, conventional nutritional management was to place the patient on a nothing-by-mouth (NPO) regimen and institute intravenous hydration. The rationale was to rest the inflamed pancreas and prevent enzyme release. Enteral or parental support should be initiated if oral intake is withheld more than 5 to 7 days.³⁹ 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.^40–42 Enteral feeding enhances immune modulation and maintenance of the intestinal barrier, and it avoids complications associated with parental nutrition. Early initiation of enteral feeding is preferred over TPN.³⁹ 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.^37,41,42 In the past, nasogastric suction was also recommended, but this intervention has not been shown to be beneficial and should be instituted only if the patient has persistent vomiting, obstruction, or gastric distention.³⁷

Systemic Complications

Acute pancreatitis can affect every organ system, and recognition and treatment of systemic complications are crucial to management of the patient (Box 30-11). The most serious complications are hypovolemic shock, acute respiratory distress syndrome (ARDS), acute kidney injury (AKI), and GI 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 ARDS and AKI. Other possible pulmonary complications include pleural effusions, atelectasis, and pneumonia.³⁷

Local Complications

Local complications include the development of infected pancreatic necrosis and pancreatic pseudocyst.19,32,38 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.

Prophylactic antibiotics may not reduce mortality in patients suspected of having necrotizing pancreatitis.⁴³ The use of IV antibiotics should not be used prophylactically but if sepsis, abscess, or biliary calculi is evident.³⁷ After the patient develops infected necrosis, however, surgical débridement is necessary.³⁶ The procedure of choice is a minimal 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. Cyst formation may result from liquefaction of a pancreatic fluid collection or from direct obstruction in the main pancreatic duct.³⁷ 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. Treatment involves drainage of the pseudocyst surgically, endoscopically, or percutaneously.^36,37,44

Providing Comfort and Emotional Support

Pain management is a major priority in acute pancreatitis. Administration of around-the-clock analgesics to achieve pain relief is essential. Morphine, fentanyl, or hydromorphine are the commonly used narcotics for pain control.³⁷ Relaxation techniques and 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 (Box 30-10). Intensive monitoring of each of the organ systems is imperative because organ failure is a major indicator of the severity of the disease.¹⁹ 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 (see Box 30-10).¹⁹

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 sustained, permanent damage to the pancreas has occurred, 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 (Box 30-9). Collaborative management of the patient with pancreatitis is outlined in Box 30-12.

Etiology

The causes of ALF include infections, medications, toxins, hypoperfusion, metabolic disorders, and surgery (Box 30-13); however, viral hepatitis and medication-induced liver damage are the predominant causes in North America. Patients are usually healthy before the onset of symptoms because ALF tends to occur in patients with no known liver history. A thorough medication and health history is imperative to determine a possible cause. The patient should be questioned about exposure to environmental toxins, hepatitis, intravenous drug use, sexual history, viral hepatitis, medication toxicity, and poisoning. Additional vascular causes such as thrombosis, ischemia, and Budd-Chiari syndrome and metabolic disorders such as Reye syndrome, Wilson disease, galactosemia, and fructose intolerance should be considered.⁴⁵

Pathophysiology

ALF is a syndrome characterized by the development of acute liver failure over 1 to 3 weeks, followed by the development of hepatic encephalopathy within 8 weeks, in a patient with a previously healthy liver. The interval between the failure of the liver and the onset of hepatic encephalopathy usually is less than 2 weeks. The underlying cause is massive necrosis of the hepatocytes.⁴⁶

Acute liver failure results in a number of derangements, including impaired bilirubin conjugation, decreased production of clotting factors, depressed glucose synthesis, and decreased lactate clearance. This results in jaundice, coagulopathies, hypoglycemia, and metabolic acidosis. Other effects of acute liver failure include increased risk of infection and altered carbohydrate, protein, and glucose metabolism. Hypoalbuminemia, fluid and electrolyte imbalances, and acute portal hypertension contribute to the development of ascites.⁴⁵ Hepatic encephalopathy is thought to result from failure of the liver to detoxify various substances in the bloodstream, and it may be worsened by metabolic and electrolyte imbalances.⁴⁶

The patient may experience a variety of other complications, including cerebral edema, cardiac dysrhythmias, acute respiratory failure, sepsis, and AKI. Cerebral edema and increased intracranial pressure (ICP) develop as a result of breakdown of the blood–brain barrier and astrocyte swelling. Circulatory failure that mimics sepsis is common in ALF and may exacerbate low cerebral perfusion pressure (CPP).⁴⁷ Hypoxemia, acidosis, electrolyte imbalances, and cerebral edema can precipitate the development of cardiac dysrhythmias. Acute respiratory failure, progressing to ARDS, intrapulmonary shunting, ventilation–perfusion mismatch, sepsis, and aspiration may attribute to the universal arterial hypoxemia.⁴⁷

Assessment and Diagnosis

Early recognition of ALF is essential. The diagnosis should include potentially reversible conditions (e.g., autoimmune hepatitis) and should differentiate ALF from decompensating chronic liver disease. Prognostic indicators such as coma grade, serum bilirubin, prothrombin time, coagulation factors, and pH should be assessed and potential causes investigated.⁴⁵

Signs and symptoms of ALF include headache, hyperventilation, jaundice, mental status changes, palmar erythema, spider nevi, bruises, and edema. The patient should be evaluated for the presence of asterixis, or “liver flap,” best described as the inability to voluntarily sustain a fixed position of the extremities. Asterixis is best recognized by downward flapping of the hands when the patient extends the arms and dorsiflexes the wrists. Hepatic encephalopathy is assessed by using a grading system that stages the encephalopathy according to the patient’s clinical manifestations (Box 30-14). Diagnostic findings include prolonged prothrombin times, elevated levels of serum bilirubin, aspartate aminotransferase (AST), alkaline phosphatase, and serum ammonia and decreased levels of serum albumin.⁴⁶ Arterial blood gases (ABGs) reveal respiratory alkalosis, metabolic acidosis, or both. Hypoglycemia, hypokalemia, and hyponatremia also may be present.^46,47

Factors I (fibrinogen), II (prothrombin), V, VII, IX, and X are produced exclusively by the liver. Prothrombin time may be the most useful of tests of these in the evaluation of acute ALF because levels may be 40 to 80 seconds above control values. Test results show decreased levels of plasmin and plasminogen and increased levels of fibrin and fibrin-split products. Platelet counts may be less than 100,000/mm³.⁴⁶

Medical Management

Medical interventions are directed toward management of the multiple system impact of ALF.

Nursing Management

Nursing management of the patient with ALF incorporates a variety of nursing diagnoses (Box 30-15). Nursing interventions include protecting the patient from injury, providing comfort and emotional support, maintaining surveillance for complications, and educating the patient and family.

Esophagectomy

Esophagectomy is usually performed for cancer of the distal esophagus and gastroesophageal junction. The technically difficult procedure involves the removal of part or all of the esophagus, part of the stomach, and lymph nodes in the surrounding area. The stomach is then pulled up into the chest and connected to the remaining part of the esophagus. If the entire esophagus and stomach must be removed, part of the bowel may be used to form the esophageal replacement (Figs. 30-5 and 30-6).⁴⁸

Pancreaticoduodenectomy

The standard operation for pancreatic cancer is a pancreaticoduodenectomy, also called the Whipple procedure. In the Whipple procedure, the pancreatic head, the duodenum, part of the jejunum, the common bile duct, the gallbladder, and part of the stomach are removed. The continuity of the GI tract is restored by anastomosing the remaining portion of the pancreas, the bile duct, and the stomach to the jejunum (Fig. 30-7).⁴⁸

Bariatric Surgery

Bariatric surgery refers to surgical procedures of the GI tract that are performed to induce weight loss. Bariatric procedures are divided into three broad types: (1) restrictive, (2) malabsorptive, and (3) combined restrictive and malabsorptive.⁴⁹ Restrictive procedures such as vertical banded gastroplasty (VBG) (Fig. 30-8A) and gastric banding (see Fig. 30-8B) reduce the capacity of the stomach and limit the amount of food that can be consumed. Malabsorptive procedures such as the biliopancreatic diversion (BPD) (see Fig. 30-8C) alter the GI tract to limit the digestion and absorption of food. The Roux-en-Y gastric bypass (RYGBP) (see Fig. 30-8D) combines both strategies by creating a small gastric pouch and anastomosing the jejunum to the pouch. Food then bypasses the lower stomach and duodenum, resulting in decreased absorption of digestive materials.⁴⁹

Preoperative Care

A thorough preoperative evaluation should be conducted to evaluate the patient’s physical status and identify risk factors that may affect the postoperative course. Because obesity is associated with a higher incidence of co-morbidities such as cardiovascular disease, hypertension, diabetes, gastroesophageal reflux, obstructive sleep apnea, and heart failure, an extensive workup may be required for the patient who underwent bariatric surgery.48,50

Surgical Considerations

Two approaches may be used for esophageal resection: transhiatal or transthoracic (see Figs. 30-5 and 30-6). In both approaches, the stomach is mobilized through an abdominal incision and then transposed into the chest. The anastomosis of the stomach to the esophagus is performed in the chest (transthoracic) or in the neck (transhiatal). The approach selected depends on the location of the tumor, the patient’s overall health and pulmonary function, and the experience of the surgeon. After surgery, the patient has a nasogastric tube in place, and it should not be manipulated because of the potential to damage the anastomosis. Those who undergo transthoracic esophagectomy have chest tubes.⁴⁸

Most bariatric procedures can be performed using an open or laparoscopic surgical technique. Although laparoscopic approaches are more technically difficult to perform, they have largely replaced open procedures because they are associated with decreased pulmonary complications, less postoperative pain, reduced length of hospital stay, fewer wound complications (e.g., infections, incisional hernia), and an earlier return to full activity.48,49 Open procedures are performed on patients who have had prior upper abdominal surgery, are morbidly obese, or who may not be able to tolerate the increased abdominal pressure associated with laparoscopic procedures.⁴⁸

Complications and Medical Management

Several complications are associated with GI surgery, including respiratory failure, atelectasis, pneumonia, anastomotic leak, deep vein thrombosis, pulmonary embolus, and bleeding. The morbidly obese patient is at even greater risk for many postoperative complications.⁴⁹

Postoperative Nursing Management

Nursing care of the patient who has had GI surgery incorporates a number of nursing diagnoses (Box 30-18). Nursing management involves interventions aimed at optimizing oxygenation and ventilation, preventing atelectasis, providing comfort and emotional support, and maintaining surveillance for complications.

Pulmonary Management

Nursing interventions in the postoperative period are focused on promoting ventilation and adequate oxygenation and preventing complications such as atelectasis and pneumonia. After the patient is extubated, deep-breathing exercises and incentive spirometry should be initiated, and the patient should perform them regularly. Early ambulation is encouraged to promote maximal lung inflation, thereby reducing the risk of pulmonary complications and the potential for pulmonary embolus.

Pain Management

It is imperative to appropriately manage the patient’s pain after GI surgery. Adequate analgesia is necessary to promote the mobility of the patient and decrease pulmonary complications. Initial pain management may be accomplished by intravenous opioid (morphine, hydromorphone) administration by means of a patient-controlled analgesia (PCA) pump, or through continuous epidural infusion of an opioid and local anesthetic (bupivacaine).⁴⁸ Oral pain medications can be started after an anastomosis leak is ruled out. Nonpharmacologic interventions such as positioning, application of heat or cold, and distraction may also be used. If the patient’s pain is not being sufficiently relieved, the pain management service should be consulted.^48,50

Nasogastric Suction Tubes

Nasogastric tubes remove fluid regurgitated into the stomach, prevent accumulation of swallowed air, may partially decompress the bowel, and reduce the patient’s risk for aspiration. Nasogastric tubes also can be used for collecting specimens, assessing the presence of blood, and administering tube feedings. The most common nasogastric tubes are the single-lumen Levin tube and the double-lumen Salem sump. The Salem sump has one lumen that is used for suction and drainage and another that allows air to enter the patient’s stomach and prevents the tube from adhering to the gastric wall and damaging the mucosa. The tube is passed through the nose into the nasopharynx and then down through the pharynx into the esophagus and stomach. The length of time the nasogastric tube remains in place depends on its use. The tube is then placed to gravity, low intermittent suction, or low continuous suction, and in rare instances, it is clamped.⁵¹

Nursing management focuses on preventing complications common to this therapy, for example, ulceration and necrosis of the nares, esophageal reflux, esophagitis, esophageal erosion and stricture, gastric erosion, and dry mouth and parotitis from mouth breathing. Interference with ventilation and coughing, aspiration, and loss of fluid and electrolytes can be critical problems. Interventions include irrigating the tube every 4 hours with normal saline, ensuring the blue air vent of the Salem sump is patent and maintained above the level of the patient’s stomach, and providing frequent mouth and nares care (Box 30-20).⁵¹

Long Intestinal Tubes

Miller-Abbott, Cantor, and Andersen tubes are examples of long, weighted-tip intestinal tubes that are placed preoperatively or intraoperatively. Their considerable length allows removal of the contents of the intestine to treat an obstruction that cannot be managed by a nasogastric tube. These tubes can decompress the small bowel and can splint the small bowel intraoperatively or postoperatively. Because progression of the tubes depends on bowel peristalsis, their use is contraindicated in patients with paralytic ileus and severe mechanical bowel obstructions.

Interventions used in the care of the patient with a long intestinal tube are similar to those with a nasogastric tube. The patient should be observed for (1) gaseous distention of the balloon section, which makes removal difficult; (2) rupture of the balloon; (3) overinflation of the balloon, which can lead to intestinal rupture; and (4) reverse intussusception if the tube is removed rapidly. Intestinal tubes should be removed slowly; usually 6 inches of the tube is withdrawn every hour.⁵¹

Feeding Tubes

Small-diameter (8- to 12-Fr [French]) flexible feeding tubes, such as Dobhoff tubes, are commonly placed at the bedside for patients who cannot take nourishment orally. The feeding tube may be inserted orally or nasally so that the tip ends up in the stomach or duodenum. To facilitate passage into the GI tract, these tubes have a weighted tungsten tip, and a guidewire is needed to prevent them from curling up in the back of the patient’s throat. A radiograph must be obtained to verify correct placement of the tube before initiating feeding.⁵² The tube should also be marked with indelible ink where it exits the mouth or nares so that tube location can be checked at 4-hour intervals.⁵²

Nursing management of the patient with a feeding tube includes prevention of complications and monitoring the tolerance of feeding. Tracheobronchial aspiration of gastric contents is a serious potential complication.52–54 Before administering medications or feedings, it is important to ensure that the tube is in the patient’s stomach or duodenum. Assessing the exit point marked on the tube helps determine whether the tube has maintained the same position. Looking for coiling in the mouth or throat can help detect upward displacement that may have occurred as a result of vomiting. The traditional practice of confirming placement by auscultating air inserted through the tube over the epigastrium is not reliable and is not recommended.^52–55 If any doubt exists about the tube’s position, a repeat radiograph should be obtained. During feedings, the head of bed should be elevated at least 30 degrees to minimize the risk of aspiration, and gastric residuals should be checked at least every 4 to 6 hours.^53,54 Large gastric residuals, cramping, and abdominal distention may indicate intolerance of feeding, and the physician should be notified.⁵⁴ Other interventions include nares and oral care and flushing the tube with water before and after medication administration to maintain patency.⁵⁴

Endoscopic Injection Therapy

Endoscopic injection therapy is used to control bleeding of ulcers. It may be performed emergently, electively, or prophylactically. An endoscope is introduced through the patient’s mouth, and endoscopy of the esophagus and stomach is performed to identify the bleeding varices or ulcers. An injector with a retractable 23- to 25-gauge needle is introduced through the biopsy channel of the endoscope. The needle then is inserted in or around the varices or into the area around the ulcer, and a liquid agent is injected (Fig. 30-9). The most commonly used agent is epinephrine, which results in localized vasoconstriction and enhanced platelet aggregation. Sclerosing agents such as ethanolamine, alcohol, and polidocanol also may be used. These agents cause an inflammatory reaction in the vessel that results in thrombosis and eventually produces a fibrous band. Repeated sclerotherapy results in the development of supportive scar tissue around the varices. Other embolic agents are used, including fibrinogen and thrombin, which when injected together react to form an active fibrin clot, and “glues” (n-butyl cyanoacrylate), which are used as a sealant to stop the bleeding.^20,24,56

Endoscopic Variceal Ligation

Endoscopic variceal ligation (EVL) involves applying bands or metal clips around the circumference of the bleeding varices to induce venous obstruction and control bleeding. EVL has replaced endoscopic sclerotherapy of variceal hemorrhage (Fig. 30-10). Between 1 and 2 days after the procedure, necrosis and scar formation promote band and tissue sloughing. Fibrinous deposits within the healing ulcer potentiate vessel obliteration. Band ligation is accomplished through endoscopy, with multiple bands placed per session.¹⁶ The procedure may be repeated on an inpatient or outpatient basis every 1 to 2 weeks until all the varices are obliterated.⁵⁶ Endoscopic variceal ligation controls bleeding in approximately 80% to 90% of the time.⁵⁶ The most common complication of endoscopic variceal ligation is the development of superficial mucosal ulcers. Varices may reoccur as local banding does not affect portal pressure.^16,57

Transjugular Intrahepatic Portosystemic Shunt

TIPS is an angiographic interventional procedure for decreasing portal hypertension. TIPS is advocated for (1) patients with portal hypertension who are also experiencing active bleeding or have poor liver reserve, (2) transplant recipients, and (3) patients with other operative risks.25,57 The TIPS procedure is usually performed by a gastroenterologist, vascular surgeon, or interventional radiologist.

Portal hypertension is confirmed by direct measurement of the pressure in the portal vein (gradient greater than 10 mm Hg). Cannulation is achieved through the internal jugular vein, and an angiographic catheter is advanced into the middle or right hepatic vein. The midhepatic vein is then catheterized, and a new route is created connecting the portal and hepatic veins using a needle and guidewire with a dilating balloon. A polytetrafluoroethylene (PTFE)–coated stent is then placed in the liver parenchyma to maintain that connection (Fig. 30-11). The increased resistance in the liver is bypassed.^25,58 TIPS may be performed on patients with bleeding varices, with refractory bleeding varices, or as a bridge to liver transplantation if the candidate becomes hemodynamically unstable. Postprocedural care should include observation for overt (cannulation site) or covert (intrahepatic site) bleeding, hepatic or portal vein laceration (resulting in rapid loss of blood volume), and inadvertent puncture of surrounding organs. Other complications include hepatic encephalopathy, liver failure, bacteremia, and stent stenosis.^25,58

Pharmacologic Agents

Many pharmacologic agents are used in the care of patients with GI disorders. Table 30-3 reviews the various agents and any special considerations necessary for administering them.

Acute Pancreatitis

Acute Liver Failure

Gastrointestinal Surgery

Therapeutic Management