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.

Neomycin or lactulose is administered to remove or decrease production of nitrogenous wastes in the large intestine. Neomycin, given orally or rectally, reduces bacterial flora of the colon. This aids in decreasing ammonia formation by decreasing bacterial action on protein in the feces. Side effects include renal toxicity and hearing impairment. Lactulose, a synthetic ketoanalogue of lactose split into lactic acid and acetic acid in the intestine, is given orally through a nasogastric tube or as a retention enema. The result is the creation of an acidic environment that decreases bacterial growth. Lactulose also traps ammonia and has a laxative effect that promotes expulsion.34

Bleeding is best controlled through prevention. Because these patients are at risk for acute gastrointestinal hemorrhage, stress ulcer prophylaxis is essential.35 If an invasive procedure (e.g., central line placement, ICP monitor) will be performed or the patient develops active bleeding, vitamin K, fresh-frozen plasma (to maintain a reasonable prothrombin time), and platelet transfusions are necessary.³⁴ Metabolic disturbances such as hypoglycemia, metabolic acidosis, hypokalemia, and hyponatremia should be monitored and treated appropriately. Prophylactic antibiotic administration may be initiated because the patient is at high risk for an infection.^33,34

The development of cerebral edema necessitates ICP monitoring. Mannitol is the only treatment shown to be of benefit in managing increased ICP in the patient with ALF, but it must be used with caution in patients with renal failure.³⁵ Other interventions to control intracranial hypertension include elevating the head of the bed (HOB) to 30 degrees, treating fever and hypertension, minimizing noxious stimulation, and correcting hypercapnia and hypoxemia.³⁵ Various experimental therapies to prevent or treat cerebral edema, such as induction of hypothermia, prophylactic phenytoin, and induction of hypernatremia, have been studied but have not improved survival.³⁵ If renal failure develops, continuous renal replacement therapy (CRRT) should be initiated.³⁵ Intubation and mechanical ventilation may be necessary as the inability to protect the airway and hypoxemia develops.³⁴ Hemodynamic instability is a common complication necessitating fluid administration and vasoactive medications to prevent prolonged episodes of hypotension. A pulmonary artery catheter may be used to guide clinical management.³⁴

If ALF continues and the patient shows no immediate signs of improvement or reversal, the patient should be considered for a liver transplant. Prompt referral to a transplantation center should be a high priority for patients experiencing ALF.^33–35

Use of benzodiazepines and other sedatives is discouraged in the ALF patient because pertinent neurological changes may be masked and hepatic encephalopathy may be exacerbated.34 These patients are often very difficult to manage because they may be extremely agitated and combative. Physical restraint may be necessary to prevent patient injury.

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 comorbidities such as cardiovascular disease, hypertension, diabetes, gastroesophageal reflux, obstructive sleep apnea, and heart failure, an extensive workup may be required for the bariatric patient.47 Before esophagectomy or pancreaticoduodenectomy, the patient may undergo multiple diagnostic tests, such as CT, positron emission tomography (PET), and endoscopic ultrasound (EUS), to determine the invasiveness of the tumor.⁴³

Two approaches may be used for esophageal resection: transhiatal or transthoracic (see Figures 22-6 and 22-7). 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 that should not be manipulated because of the potential to damage the anastomosis. Those who undergo transthoracic esophagectomy have one or more chest tubes.^43,44

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.^46,48 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.⁴⁴

Several complications are associated with gastrointestinal 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.46,47

Liver transplantation must be considered for any patient who suffers from irreversible acute or chronic liver disease that is progressive and for which there is no therapy of established efficacy. Diseases of the liver may be categorized as chronic, vascular, acute liver failure, and include inborn errors of metabolism and hepatic malignancies. Box 22-9 lists the most common diseases seen in patients who undergo liver transplantation. In the United States, the single most common indication for liver transplantation in adults is chronic viral hepatitis C.⁵⁰

Candidate selection is an important aspect of transplantation. Given the shortage of available organs, the transplantation team must have reasonable assurance of a successful outcome. The timing of transplantation is of utmost importance. The patient must not be so ill as to be unable to survive the surgery but yet be experiencing deterioration in the quality of life. Body mass index (BMI) plays a role in posttransplantation survival. Patients who are underweight (BMI < 20) or morbidly obese (BMI > 40) are at greater risk for death after transplantation.⁵¹ In general, liver transplantation is not to be offered to persons in the following groups:

The absolute contraindications listed in Box 22-10 fall under these four specific categories.

Having one relative contraindication may not rule out transplantation, but having several predicts poor outcome. Chronological age is less important than physiological age. Reports of transplantation in older patients describe favorable results.⁵² Certain diseases can recur after transplantation, including viral hepatitis,⁵³ sclerosing cholangitis,⁵⁴ and biliary malignancies.⁵⁵ In the case of viral hepatitis, serologic indicators of viral replication are monitored closely. In the presence of aggressively replicating virus and in certain malignancies, it is in the patient’s best interest not to proceed to transplantation, because it would actually hasten death. Multicenter protocols are important in evaluating the outcomes and efficacies of transplantations in patients with diseases that recur. The decision to offer liver transplantation to any patient must be based on evaluation criteria, which vary among institutions and are modified as advances in technical ability, immunosuppression, and perioperative management continue. In the absence of complications, the average hospital stay after liver transplantation is 7 to 14 days.

The candidate for liver transplantation undergoes a thorough evaluation to determine the cause and severity of the liver disease, to establish the need for transplantation rather than other interventions, and to identify objective indications and contraindications. Evaluation begins with a carefully elicited patient history (Box 22-11). A comprehensive approach includes laboratory, radiographic, and diagnostic testing and multidisciplinary consultations (Box 22-12). Not every patient undergoes every test and consultation. Careful history taking and a good physical examination direct the initial diagnostic testing. For instance, a patient with a past history of malignancy would undergo extensive testing to rule out metastases, whereas a patient with acute liver failure may have a more abbreviated workup that is focused on determining the cause and potential for hepatic recovery.⁵⁶

During the workup, the candidate’s support systems are evaluated by the entire transplantation team, which includes the surgeon, the hepatologist, the clinical transplantation nurse coordinator, the social worker, the dietitian, and the financial counselor. Other services, such as cardiology, nephrology, psychiatry, gynecology, anesthesia, infectious disease, endocrinology, hematology, rheumatology, and oral surgery or dentistry, may also be included in the evaluation. Ideally, all immunizations are brought up to date in an attempt to minimize postoperative infections. The patient and family receive education regarding the evaluation, waiting list, surgery, postoperative management including immunosuppression, and long-term follow-up. At the conclusion of the evaluation, one of several outcomes is possible: (1) the patient is deemed a transplant candidate, (2) the patient is deemed not a candidate, or (3) the patient may be a candidate sometime in the future if certain criteria are met. These criteria may be of a physical nature (e.g., it is too early in the disease process to list now, in which case the patient will be re-evaluated at set intervals), or they may be of a psychosocial nature (e.g., the patient must attend a formal alcohol or drug rehabilitation program or undergo treatment of depression).⁵⁶

After candidacy has been determined and the patient is ready for transplantation, his or her social security number is entered into the national computer system operated by United Network for Organ Sharing (UNOS). Objective criteria are used to place a patient on the waiting list. These data are used in a formula to determine the patient’s score, which is directly associated with the patient’s risk of death within 3 months (the higher the score, the higher the risk).

The patient with end-stage liver disease who is awaiting a transplant may pose one of the greatest care challenges in the critical care unit. Hepatic encephalopathy, coagulopathies, portal hypertension, severe fluid and electrolyte imbalances, cardiac compromise, and renal deterioration are not uncommon. Frequent mental status assessments are important in determining the patient’s continued candidacy for transplantation. Hepatic encephalopathy may improve with the administration of antibiotics and laxatives, or the patient may proceed to stage IV coma. Protection of the airway is especially important in an encephalopathic patient who is not intubated. In these circumstances, if hematemesis or vomiting occurs, intubation and use of paralytic agents may be necessary to protect the patient’s airway. Diagnostic studies may be needed to evaluate the possibility of an intracranial bleed. The head of the patient’s bed is maintained at 30 to 45 degrees to avoid even slight increases in intracranial pressure. Patients who have chronic liver disease also have nutritional deficits. They require supplements of the fat-soluble vitamins (A, D, E, and K), may be on protein restriction to reduce serum ammonia levels, and may experience severe muscle wasting.33

Consequences of portal hypertension must be corrected. Gastrointestinal hemorrhage from varices may respond to administration of propranolol or to procedures such as banding and sclerotherapy. Portal hypertension may be reduced by transjugular intrahepatic portosystemic shunting (TIPS) in interventional radiology. Rarely, the patient may need to undergo surgical intervention with a vascular shunt created between the portacaval system and the mesangial, splenic, or renal vascular system. Patients with massive ascites usually have total body fluid overload but are intravascularly contracted and require sodium restriction and administration of colloidal fluids (e.g., albumin) along with diuretics.

Careful documentation of fluid intake and output, daily weight determinations, and frequent measurement of vital signs are needed to monitor fluid status. Ascites can interfere with lung expansion and can compromise oxygenation. Patients with large, distended abdomens also find adequate oral nutrition difficult. Use of diuretics to control ascites is common but can compromise kidney function or even worsen hepatorenal syndrome. Paracentesis (removal of ascites) may be required for intractable ascites. However, frequent large-volume paracentesis procedures can contribute to renal demise and cardiovascular compromise related to fluid volume shifts.

Spontaneous bacterial peritonitis can be manifested in the patient with end-stage liver disease by an acute decline in the hepatic and renal function accompanied by fever, abdominal pain, and hepatic encephalopathy. The paracentesis fluid shows increased white blood cells with or without a positive culture. Patients are treated aggressively with antibiotics and are temporarily deferred from transplantation during treatment for and recovery from bacterial peritonitis.

In very urgent situations, the donor blood type (e.g., type A) may not be compatible with that of the recipient (e.g., type O). Despite this incompatibility, such liver transplantations can be successful. There may be some early postoperative complications, such as mild hemolysis, higher incidence of acute cellular rejection, and increased postoperative hepatic vascular and biliary complications, but innovative use of immunosuppressive regimens and plasmapheresis have improved graft survival of patients with recipient-donor ABO incompatibility.61 Extended-criteria donor livers that are otherwise unremarkable—such as those with a cold ischemia time longer than 12 hours or those from donors older than 60 years—are expanding the donor pool and shortening waiting times.⁶²

Living Donor Liver Transplantation (LDLT) began in 1989 with adult-to-child donations, commonly from a parent to his or her infant. The left lateral hepatic lobe is resected, leaving the donor with the larger mass of liver remaining.63 In such cases, the risks to the healthy donor are thought to be outweighed by the benefits of having a healthy child.⁶⁴ Adult-to-adult LDLT donation began in the 1990s. The whole left hepatic lobe or right hepatic lobe is resected, taking 30% to 60% of the liver mass from the live donor.⁶³ Complications for the donor after partial hepatectomy are usually of low severity. The most common ones are bile leak, bacterial infection, incisional hernia, pleural effusion, neuropraxia (temporary nerve dysfunction), wound infection, and abdominal abcess.^59,64 More serious potential complications for the liver donor include portal vein thrombosis, inferior vena cava thrombosis, and death.^59,64 Critical care nurses play an important role in caring for these donors and must be vigilant in assessing for complications and initiating early interventions.

Liver transplantation surgery is lengthy and technically difficult, often lasting 4 to 12 hours. The procedure involves the combined efforts of surgeons, anesthesiologists, nurse anesthetists, operating room nurses and technicians, perfusionists, and personnel from the blood bank and laboratory and radiology departments, among others. The patient is taken to the operating room for anesthesia induction, insertion of large-bore intravenous catheters that allow high-volume fluid infusion, and insertion of a pulmonary artery catheter for hemodynamic monitoring. Continuous renal replacement may be continued or initiated in the operating room by a filter-trained critical care or dialysis nurse. Other devices, such as an arterial line, a nasogastric tube, and a urinary drainage catheter, are also inserted. The patient is positioned on the operating room table in such a way as to minimize pressure that could cause ischemia and chronic injury to tissue and peripheral nerves. Liver transplantation surgery can be divided into three stages: (1) recipient hepatectomy, (2) vascular anastomoses with donor liver, and (3) biliary anastomosis.65

Recipient Hepatectomy

Stage 1 is the longest and most difficult part of the surgery, because it involves removal of the native liver. It is complicated even more by coagulopathies, adhesions, portal hypertension, and venous collaterals. Before completion of this stage, the patient may be placed on venovenous bypass (Figure 22-9), although not all patients require this procedure. A centrifugal pump cycles the blood out through iliac and portal vein cannulas and returns it to the central circulation through the axillary or subclavian vein. Advances in surgical techniques, anesthesia, and fluid management have shortened the length of surgery enough to warrant elimination of venovenous bypass in some cases.⁶⁶

Biliary Anastomosis

Stage 3 can be achieved by choledochojejunostomy (bile duct to jejunum) or by choledochocholedochostomy (bile duct to bile duct). Choledochojejunostomy is performed in patients who have diseased bile ducts, such as those with biliary atresia or sclerosing cholangitis. It is also known as a Roux-en-Y procedure and is shown in Figure 22-10. The choledochocholedochostomy is performed in patients who have a healthy and intact common bile duct and is shown in Figure 22-11. The patient returns from surgery with or without an external stent or T-tube that is connected to a bag into which bile drains. Patients who do not have external biliary tubes may have an internal stent inserted in the bile duct across the biliary anastomosis. Eventually, the internal stent moves and is passed with the stool.⁶⁶

A number of different antiulcer agents are commonly used in the critical care setting, including H₂-antagonists, gastric PPIs, and gastric mucosal agents.70 H₂-antagonists are used to decrease the volume and concentration of gastric secretions and control gastric pH, decreasing the incidence of stress-related upper gastrointestinal bleeding. These agents work by blocking histamine stimulation of the H₂-receptors on the gastric parietal cells, reducing acid production. Although these drugs may be administered orally, intramuscularly, or intravenously, they usually are given intravenously in the critical care setting. Proton-pump inhibitors decrease gastric acid secretion by binding to the proton pump, blocking the release of acid from the gastric parietal cells. PPIs are potent acid inhibitors and have greater suppressive ability than the H₂-agonists.^71,72

Unlike H₂-antagonists or PPIs, sucralfate does not affect gastric acid concentration but rather exerts its action locally. Sucralfate reacts with hydrochloric acid to form a sticky, paste-like substance that adheres to the surface of the ulcer and shields it from pepsin, acid, and bile. Sucralfate predominantly binds to damaged gastrointestinal mucosa, with minimal adherence to normal tissue.⁷² It is administered orally or through a gastric tube. Sucralfate should not be crushed but may be dissolved in 10 mL of water to form a slurry. It is also available as a suspension.

Vasopressin is used to control gastric ulcer and variceal bleeding. It is administered intraarterially, through a catheter inserted into the right or left gastric artery (through the femoral artery, aorta, and celiac trunk) or intravenously. It causes splanchnic and systemic vasoconstriction, subsequently reducing portal blood flow and pressure.71 A major side effect of the drug is systemic vasoconstriction, which can result in cardiac ischemia, chest pain, hypertension, acute heart failure, dysrhythmias, phlebitis, bowel ischemia, and cerebrovascular accident. These side effects can be offset with concurrent administration of nitroglycerin. Other complications include bradycardia and fluid retention. Nursing responsibilities associated with the use of this therapy include maintenance of a patent infusion line and continuous monitoring for vasoconstrictive complications of therapy.¹⁸

Somatostatin is a peptide that is administered parenterally in the acutely bleeding, cirrhotic patient. It reduces splanchnic vasodilation and portal pressure through the inhibition of secretion of various vasodilator hormones, and it is as effective as vasopressin in treating variceal bleeding with minimal side effects. Octreotide is a commonly used, long-acting synthetic analogue of somatostatin.18,71