Assessment and Diagnosis

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GI hemorrhage results in hypovolemic shock, initiation of the shock response, and development of multiple organ dysfunction syndrome if left untreated (Figure 22-2).⁷ However, the most common cause of death in cases of GI hemorrhage is exacerbation of the underlying disease, not intractable hypovolemic shock.

Assessment and Diagnosis

The initial clinical presentation of the patient with acute GI 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 GI hemorrhage.^5,18

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

FIG 22-1 Varices Related to Portal Hypertension. Portal vein, its major tributaries, and the most important shunts (col- lateral veins) between the portal and caval systems. (From Monahan FD, et al. Phipps’ Medical-Surgical Nursing: Con- cepts and Clinical Practice. 8th ed. St. Louis: Mosby; 2007.)

Esophageal varices Short gastrics

Splenic Coronary Inferior mesenteric

Hemorrhoidal Superior mesenteric

Portal

Veins of Sappey Azygos UPPER

GASTROINTESTINAL TRACT

LOWER

GASTROINTESTINAL TRACT

• Peptic ulcer disease • Diverticulosis

• Stress-related erosive syndrome

• Angiodysplasia

• Esophagogastric varices • Neoplasm

• Mallory-Weiss tear • Inflammatory bowel disease

• Esophagitis • Trauma

• Neoplasm • Infectious colitis

• Aortoenteric fistula • Radiation colitis

• Angiodysplasia • Ischemia

• Aortoenteric fistula

• Hemorrhoids

BOX 22-1 Causes of Acute

Gastrointestinal Hemorrhage

disease severity and variceal size, but overall, bleeding occurs in 25% to 30% of patients within 2 years of diagnosis, and 20% to 30% mortality from each bleeding episode.^16,17

Pathophysiology

GI hemorrhage is a life-threatening disorder that is characterized by acute, massive bleeding. Regardless of the cause, acute

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

CLASS

BLOOD LOSS (%)

CLINICAL SIGNS AND SYMPTOMS

1 ≤15 Pulse rate: normal or

<100 beats/min (supine) Capillary refill <3 seconds 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

TABLE 22-1 Clinical Classification of Hemorrhage

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FIG 22-2 Concept Map for Gastrointestinal Hemorrhage. (Illustrated by Elaine B. Kennedy, EdD, RN.)

Esophogastric varices Peptic ulcer disease

Stress-related mucosal disease (SRMD) Other upper and lower GI etiologies

GASTROINTESTINAL HEMORRHAGE Class 2 15–30% blood loss Decreased blood volume Compensatory contriction of peripheral arteries Increased anerobic metabolism Renin, ADH, aldosterone released Blood accumulating in the GI tract Digestion of blood protein Class 3 30–40% blood loss Decreased blood flow to vital organs Non-vital organs hypoxic/anoxic Decreased blood flow to kidneys Cellular damage and death Class 4 Greater than 40% blood loss Cellular deterioration continues to worsen Multiple Organ System Dysfunction Syndrome (MODS) Heart, brain, kidneys, GI tract cease to function Hematemesis Hematochezia and melena Pulse 100 BPM Systolic BP100 mm Hg Respiratory rate increased Skin cool, pale, sweaty Peripheral pulses rapid and thready Change in level of consciousness Increased peristalsis and diarrhea Hct, Hgb decreased BUN increased Slow capillary refill Lethargy Bowel sounds absent Urinary output 5–15 mL/hr PaO2, PaCO2, pH decreased Serum Na, K increased Sluggish pupil response Coma Heart rate decreases Dysrhythmias, angina, hypotension Anuria Abdominal pain

Progresses to Progresses to

Leads to

Etiologies Blood, blood products Intravenous fluids Antacids H2-receptor blockers Cytoprotective agents Proton pump inhibitors

Vasopressin

Decreased cardial output R/T alterations in preload

Manage fluid replacement Control bleeding-gastric lavage Provide safe care for patient with endoscopic injection therapy, transjugular intrahepatic portosystemic shunt (TIPS) or who has experienced surgery to eliminate source of bleeding Surveillance Monitor vital signs Monitor cardiac rhythm Monitor urinary output Surveillance Monitor gastric perforation Protect skin from injury Turn frequently

Deficient fluid volume R/T absolute loss Risk for ineffective gastrointestinal perfusion

Pathophysiology

Etiology Nursing Diagnosis Nursing InterventionsAssessments

KEY Medication

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Peptic ulcer disease. In the patient with GI hemorrhage related to peptic ulcer disease, bleeding hemostasis may be accomplished by endoscopic injection therapy in conjunc- tion with thermal or hemostatic clips.²⁰ 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.⁶ 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.¹⁹

Stress-related mucosal disease. In the patient with GI 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.¹⁹

Esophagogastric varices. In acute variceal hemorrhage, control of bleeding may be initially accomplished through the use of pharmacologic agents and endoscopic therapies. Intra- venous 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 sclero- therapy (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 (Figure 22-3).^23,24

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 fiberop- tic 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 view the GI tract clearly because of continued active bleeding.¹⁹

Medical Management

To reduce mortality related to GI hemorrhage, patients at risk should be identified early, and interventions should be imple- mented to reduce gastric acidity and support the gastric mucosal defense mechanisms. Management of the patient at risk for GI hemorrhage should include prophylactic administration of pharmacologic agents for neutralization of gastric acids. These agents include antacids, histamine-2 (H2) antag- onists, cytoprotective agents, and proton pump inhibitors (PPIs).^5,22 Priorities in the medical management of the patient with GI hemorrhage include airway protection, fluid resuscitation to achieve hemodynamic stability, correction of co-morbid conditions (e.g., coagulopathy), therapeutic procedures to control or stop bleeding, and diagnostic procedures to determine the exact cause of the bleeding.^5,21 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 infu- sions of crystalloids, blood, and blood products.²² Hemody- namic 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.

FIG 22-3 Anatomic Location of the Transjugular Intrahe- patic Portosystemic Shunt (TIPS). (From Vargas HE, et al.

Management of portal hypertension-related bleeding. Surg Clin North Am. 1999;79:1.)

Esophagus

Liver Stomach

Varices Spleen

Splenic vein Coronary vein

Portal vein Hepatic

vein

Shunt

Inferior vena cava

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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

Nursing Management

All critically ill patients should be considered at risk for stress ulcers and, therefore, GI hemorrhage. Routine assessment of gastric fluid pH monitoring is controversial.^12,28 Maintaining the pH between 3.5 and 4.5 is a goal of prophylactic therapy.

Gastric pH measurements made with litmus paper or direct nasogastric tube probes may be used to assess gastric fluid pH and the effectiveness or need for prophylactic agents.²⁸ Patients at risk also should be assessed for the presence of bright red or coffee grounds emesis, bloody nasogastric aspi- rate, and bright red, black, or dark red stools.⁴ Any signs of bleeding should be promptly reported to the physician.

Nursing management of a patient experiencing acute GI hemorrhage incorporates a variety of nursing diagnoses (Box 22-2). Nursing priorities are directed toward 1) Surgical Intervention

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

Peptic ulcer disease. Surgical intervention is required to control bleeding in a minority of patients.²⁵ 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.²⁶

Stress-related mucosal disease. In the past, several operative procedures were used to control bleeding from SRMD. Because of the advent of stress ulcer prophylaxis, a marked decrease occurs in the incidence of hemorrhage from SRMD.²²

Esophagogastric varices. If medical treatment is unsuc- cessful and angiographic interventional TIPS procedure is not available, operative procedures to control bleeding gas- troesophageal varices may be undertaken. Though rarely performed, operative interventions focus on some form of shunting (Figure 22-4).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

FIG 22-4 Portosystemic Shunt Operative Procedures. (From Copstead LC, Banasik JL. Patho- physiology. 4th ed. St. Louis: Saunders; 2010.)

Inferior vena cava

Normal (without anastomosis) Portacaval side-to-side shunt Portacaval end-to-side shunt

Cavomesenteric shunt Central splenorenal shunt Distal splenorenal shunt Portal vein

Left renal vein Mesenteric vein Splenic vein

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be referred to an alcohol cessation program (Box 22-3). Col- laborative management of the patient with acute GI hemorrhage is outlined in Box 22-4.

ACUTE PANCREATITIS Description and Etiology

Acute pancreatitis is an inflammation of the pancreas that produces exocrine and endocrine dysfunction that may also involve surrounding tissues, remote organ systems, or both.

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

• Gastrointestinal hemorrhage

• Specific cause

• Precipitating factor modification

• Interventions to reduce further bleeding episodes

• Importance of taking medications

• Lifestyle changes

• Stress management

• Diet modifications

• Alcohol cessation

• Smoking cessation

Additional information for the patient can be found at the following websites:

• Alcoholics Anonymous: http://www.aa.org

• International Foundation for Functional Gastrointestinal Disorders: http://www.iffgd.org

• Healthfinder—U.S. Department of Health and Human Ser- vices: http://healthfinder.gov

• Web MD: http://www.webmd.com

BOX 22-3 PATIENT EDUCATION PRIORITIES

Acute Gastrointestinal Hemorrhage

• Initiate fluid resuscitation to achieve hemodynamic stability.

• Crystalloids

• Colloids

• Blood and blood products

• Determine the cause of the bleeding.

• Gastric lavage

• Control bleeding.

• Endoscopic interventions

• Vasopressin, somatostatin, octreotide

• Transjugular intrahepatic portosystemic shunting

• Surgery (last resort)

• Provide comfort and emotional support.

• Maintain surveillance for complications.

• Hypovolemic shock

• Gastric perforation

BOX 22-4 COLLABORATIVE MANAGEMENT Acute Gastrointestinal Hemorrhage administering volume replacement, 2) controlling the

bleeding, 3) providing comfort and emotional support, 4) maintaining surveillance for complications, and 5) educat- ing 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.¹

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.²⁹

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.³⁰

Educating the Patient and Family

Early in the hospital stay, the patient and family should be taught about acute GI 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

BOX 22-2 NURSING DIAGNOSIS PRIORITIES

• Deficient Fluid Volume, related to absolute loss, p. 583

• Decreased Cardiac Output, related to alterations in preload, p. 579

• Imbalanced Nutrition: Less Than Body Requirements, related to lack of exogenous nutrients and increased metabolic demand, p. 593

• Powerlessness, related to health care environment or illness-related regimen, p. 600

• Deficient Knowledge, related to lack of previous exposure to information, p. 585 (see Patient Education, Box 22-3)

Acute Gastrointestinal Hemorrhage

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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, dis- ruption 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 22-7). 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 incapacitat- ing. 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, dia- phoresis, weakness, tachypnea, hypotension, and tachycardia.

the other 20% develop severe acute necrotizing pancreatitis.³¹ Reported mortality rates for acute pancreatitis range from 2%

to 15% overall, with a steadily increasing rate of about 20,000 deaths per year in the United States.^32,33 Several prognostic scoring systems have been developed to predict the severity of acute pancreatitis. One of the most commonly used is Ranson criteria³⁴ (Box 22-5). 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%.^34-36

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 22-6). 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 initi- ates 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

• Biliary disease (stones, sludge, common bile duct obstruction)

• Toxins (ethyl alcohol, methyl alcohol, scorpion venom, parathion)

• Smoking

• Medications

• Hypercalcemia (hyperparathyroidism)

• Hyperlipidemia

• Tumors

• Infections (bacterial, viral, parasitic)

• Trauma (abdominal, surgical, endoscopic)

• Hypoperfusion

• Vasculitis

• Pregnancy

• Hypothermia

• Sphincter of Oddi dysfunction

• Autoimmune diseases

• Ampullary stenosis

• Idiopathic cause

BOX 22-6 Causes of Acute Pancreatitis

From Latifi R, et al. Nutritional management of acute and chronic pancreatitis. Surg Clin North Am. 1991: 71:583.

At Admission

• Age >55 years

• Hypotension

• Abnormal pulmonary findings

• Abdominal mass

• Hemorrhagic or discolored peritoneal fluid

• Increased serum LDH levels (>350 units/L)

• AST >250 units/L

• Leukocytosis (>16,000/mm³)

• Hyperglycemia (>200 mg/dL; no diabetes history)

• Neurologic deficit (confusion, localizing signs) During Initial 48 Hours of Hospitalization

• Fall in hematocrit >10% with hydration or hematocrit <30%

• Necessity for massive fluid and colloid replacement

• Hypocalcemia (<8 mg/dL)

• Arterial PO2 <60 mm Hg with or without acute respiratory distress syndrome

• Hypoalbuminemia (<3.2 mg/dL)

• Base deficit >4 mEq/L

• Azotemia

BOX 22-5 Ranson’s Criteria for Estimating the Severity of Acute Pancreatitis

AST, Aspartate aminotransferase; LDH, lactate dehydrogenase;

PO2, partial pressure of oxygen.

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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.³⁵ Careful monitoring for systemic and local complications is critical.

Fluid Management

Because pancreatitis is 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 Depending on the extent of fluid loss and hemorrhage, the

patient may exhibit signs of hypovolemic shock.^19,37

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 sign (gray-blue discoloration of the flanks) and Cullen sign (discoloration of the umbilical region); however, they are rare and usually seen several days into the illness.¹⁹ A palpable abdominal mass indicates the presence of a pseudocyst or abscess.¹⁹

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 emergen- cies, 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. A marker of severity may be determined with a serum cross-reactive (C-reactive) protein level.^19,38 Leukocy- tosis, hypocalcemia, hyperglycemia, hyperbilirubinemia, and hypoalbuminemia may also be present (Table 22-2).^19,36,38 Diagnostic Procedures

An abdominal ultrasound scan is obtained as part of the diagnostic evaluation to determine the presence of biliary stones. Contrast-enhanced computed tomography (CT) is considered the gold standard for diagnosing pancreatitis and for ascertaining the overall degree of pancreatic inflammation and necrosis.^19,32

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

• Pain

• Vomiting

• Nausea

• Fever

• Abdominal distention

• Abdominal guarding

• Abdominal tympany

• Hypoactive or absent bowel sounds

• Severe disease

• Peritoneal signs

• Ascites

• Jaundice

• Palpable abdominal mass

• Grey Turner sign

• Cullen sign

• Signs of hypovolemic shock

BOX 22-7 Presenting Clinical Manifestations of Acute Pancreatitis

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

STUDY

FINDING IN PANCREATITIS Laboratory Studies

Serum amylase Elevated

Serum isoamylase Elevated

Urine amylase Elevated

Serum lipase (if available) Elevated

Serum triglycerides Elevated

Cross-reactive protein 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)

TABLE 22-2 Laboratory Tests and Diagnostic Procedures for Acute Pancreatitis

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inflamed pancreas and prevent enzyme release. Enteral or parenteral support should be initiated if oral intake is with- held 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 parenteral 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 tol- erate 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 22-8). 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 are evident.³⁷ After the patient develops infected necrosis, however, surgical debridement is necessary.³⁶ The procedure of choice is a minimally invasive necrosectomy, which entails careful debridement 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 lique- faction 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 perito- nitis; 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, endoscopi- cally, or percutaneously.^36,37,44

Nursing Management

Nursing management of the patient with pancreatitis incorporates a variety of nursing diagnoses (Box 22-9). Nursing priorities are directed toward 1) providing comfort and emotional support, 2) maintaining surveillance for com- plications, and 3) educating the patient and family.

Respiratory

• Early hypoxemia

• Pleural effusion

• Atelectasis

• Pulmonary infiltration

• Acute respiratory distress syndrome

• Mediastinal abscess Cardiovascular

• Hypotension and shock

• Pericardial effusion

• ST-T changes Renal

• Acute tubular necrosis

• Oliguria

• Renal artery or vein thrombosis Hematologic

• Disseminated intravascular coagulation

• Thrombocytosis

• Hyperfibrinogenemia Endocrine

• Hypocalcemia

• Hypertriglyceridemia

• Hyperglycemia Neurologic

• Fat emboli

• Psychosis

• Encephalopathy and coma Ophthalmic

• Purtscher’s retinopathy (sudden blindness) Dermatologic

• Subcutaneous fat necrosis Gastrointestinal or Hepatic

• Hepatic dysfunction

• Obstructive jaundice

• Stress ulceration

• Erosive gastritis

• Paralytic ileus

• Duodenal obstruction

• Pancreatic

• Pseudocyst

• Phlegmon

• Abscess

• Ascites

• Bowel infarction

• Massive intraperitoneal bleed

• Perforation

• Stomach

• Duodenum

• Small bowel

• Colon

BOX 22-8 Complications of Acute Pancreatitis

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BOX 22-9 NURSING DIAGNOSIS PRIORITIES

• Acute Pain, related to transmission and perception of cuta- neous, visceral, muscular, ischemia impulses, p. 574

• Deficient Fluid Volume, related to relative fluid loss, p. 584

• Ineffective Breathing Pattern, related to decreased lung expansion, p. 598

• Anxiety, related to threat to biologic, psychologic, or social integrity, p. 576

Acute Pancreatitis

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 hydromor- phone are the commonly used narcotics for pain control.³⁷ Relaxation techniques and the knee-chest position can also assist in pain control.

The patient must be routinely monitored for signs of local or systemic complications (Box 22-8). 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 (Box 22-11).¹⁹

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, per- manent 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 22-10). Collaborative management of the patient with pancreatitis is outlined in Box 22-12.

ACUTE LIVER FAILURE Description and Etiology

Acute liver failure (ALF) is a life-threatening condition characterized by severe and sudden liver cell dysfunction, coagulopathy, and hepatic encephalopathy.⁴⁵ Although uncommon, ALF is associated with a mortality rate as high as 40%, and it usually occurs in patients without preexisting liver disease.⁴⁵ Because liver transplantation is one of the few definitive treatments, the patient with ALF should be transferred to a critical care unit and strongly considered for referral to a major medical center where transplantation services are available.⁴⁵

• Pancreatitis

• Specific cause

• Precipitating factor modification

• Interventions to reduce further episodes

• Importance of taking medications

• Lifestyle changes

• Diet modification

• Stress management

• Alcohol cessation

• Diabetes management, if needed

Additional information for the patient can be found at the following websites:

• The Pancreatitis Association, Inc.: http://pancassociation.org

• Alcoholics Anonymous: http://www.aa.org

• International Foundation for Functional Gastrointestinal Disorders: http://www.iffgd.org

• Healthfinder—U.S. Department of Health and Human Ser- vices: http://healthfinder.gov

• Web MD: http://www.webmd.com

BOX 22-10 PATIENT EDUCATION PRIORITIES

Acute Pancreatitis

The causes of ALF include infections, medications, toxins, hypoperfusion, metabolic disorders, and surgery (Box 22-13);

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

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

Symptoms

• Persistent abdominal pain

• Abdominal tenderness Signs

• Prolonged fever

• Abdominal distention

• Palpable abdominal mass

• Vomiting Diagnostics

• Laboratory findings

• Increased white blood cell count

• Persistent elevation of serum amylase

• Hyperbilirubinemia

• Elevated alkaline phosphatase level

• Positive culture and Gram stain

• Radiography or computed tomography findings

• Pancreatic inflammation or enlargement

• Necrosis

• Cystic or mass lesions

• Fluid accumulations

• Pseudocyst abscess

BOX 22-11 Signs and Symptoms of Pancreatic Infection

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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, hyperven- tilation, jaundice, mental status changes, palmar erythema, spider nevi, bruises, and edema. The patient should be evalu- ated for the presence of asterixis, or “liver flap,” best described as the inability to sustain a fixed position of the extremities voluntarily. Asterixis is best recognized by downward flap- ping 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 accord- ing to the patient’s clinical manifestations (Box 22-14).

Infections

• Hepatitis A, B, C, D, E, non-A, non-B, non-C

• Herpes simplex virus (types 1 and 2)

• Epstein-Barr virus

• Varicella zoster

• Dengue fever virus

• Rift Valley fever virus Medications or Toxins

• Industrial substances (chlorinated hydrocarbons, phosphorus)

• Amanita phalloides (mushrooms)

• Aflatoxin (a toxic metabolite of fungus)

• Medications (isoniazid, rifampin, halothane, methyldopa, tetracycline, valproic acid, monoamine oxidase inhibitors, phenytoin, nicotinic acid, tricyclic antidepressants, isoflu- rane, ketoconazole, trimethoprim-sulfamethoxazole, sul- fasalazine, pyrimethamine, octreotide)

• Acetaminophen toxicity

• Cocaine Hypoperfusion

• Venous obstructions

• Budd-Chiari syndrome

• Veno-occlusive disease

• Ischemia

Metabolic Disorders

• Wilson disease

• Tyrosinemia

• Heat stroke

• Galactosemia Surgery

• Jejunoileal bypass

• Partial hepatectomy

• Liver transplantation failure Other Causes

• Reye’s syndrome

• Acute fatty liver of pregnancy

• Massive malignant infiltration

• Autoimmune hepatitis

BOX 22-13 Causes of Acute Liver Failure

• Ensure adequate circulating volume.

• Provide nutritional support.

• Correct metabolic alterations.

• Minimize pancreatic stimulation.

• Provide comfort and emotional support.

• Maintain surveillance for complications.

• Multiple organ dysfunction syndrome

BOX 22-12 COLLABORATIVE MANAGEMENT Acute Pancreatitis

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’s 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, coagu- lopathies, 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 blood- stream, 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

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be used with caution in patients with renal failure to avoid hyperosmolarity.⁴⁷ Other interventions to control ICP include elevating the head of the bed (HOB) to 30 degrees, treating fever and hypertension, minimizing noxious stimulation, and correcting hypercapnia and hypoxemia.²⁵ Renal failure develops in 70% of patients with ALF, and continuous renal replacement therapy (CRRT) provides renal support.²⁵ Hemodynamic instability is a common complication neces- sitating fluid administration and vasoactive medications to prevent prolonged episodes of hypotension. A pulmonary artery catheter may be used to guide clinical management.⁴⁶

If ALF continues and the patient shows no immediate signs of improvement or reversal, the patient should be considered for a liver transplantation. Prompt referral to a transplantation center should be a high priority for patients experiencing ALF.^25,45

Nursing Management

Nursing management of the patient with ALF incorporates a variety of nursing diagnoses (Box 22-15). Nursing priorities are directed toward 1) protecting the patient from injury, 2) providing comfort and emotional support, 3) maintain- ing surveillance for complications, and 4) educating the patient and family.

Use of benzodiazepines and other sedatives is discouraged in the patient with ALF because pertinent neurologic changes may be masked and hepatic encephalopathy may be exacer- bated.⁴⁷ These patients are often very difficult to manage because they may be extremely agitated and combative. Phys- ical restraint may be necessary to prevent injury to the patient.

As the neurologic condition worsens, respiratory depression and arrest can occur quickly. Continuous pulse oximetry monitoring and ABG analysis are helpful in assessing ade- quacy of respiratory efforts. A thorough neurologic assessment should be performed at least every hour.

Early in the patient’s hospital stay, the patient and family should be taught about ALF and its causes and treatment. As patient discharge is imminent, teaching should focus on the interventions necessary for preventing the recurrence of the 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 plas- minogen 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.

Ammonia Levels

Antibiotics such as neomycin, metronidazole, rifaximin, or lactulose, which is the gold standard, are administered to remove or decrease production of nitrogenous wastes in the large intestine. Antibiotics reduce bacterial flora of the colon.

This aids in decreasing ammonia formation by decreasing bacterial action on the protein in 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 results in ammonia being drawn out of the portal circulation. Lactulose has a laxative effect that pro- motes expulsion.^46,47

Complications

Bleeding is best controlled through prevention. 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.²⁵ Metabolic dis- turbances 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.²⁵ The development of cerebral edema necessitates ICP monitoring. Treatment with mannitol has been shown to be of benefit in managing ICP in the patient with ALF, but it must

I. Euphoria or depression, mild confusion, slurred speech, disordered sleep rhythm; slight asterixis and normal elec- troencephalogram (EEG)

II. Lethargy, moderate confusion; marked asterixis and abnormal EEG

III. Marked confusion, incoherent speech, sleeping but arousable; asterixis present and abnormal EEG

IV. Coma; initially responsive to noxious stimuli, later unre- sponsive; asterixis absent and abnormal EEG

BOX 22-14 Staging of Hepatic

Encephalopathy ^{BOX 22-15} NURSING DIAGNOSIS PRIORITIES

• Impaired Gas Exchange, related to ventilation/perfusion mismatching or intrapulmonary shunting, p. 594

• Decreased Cardiac Output, related to alterations in preload, p. 579

• Risk for Infection, p. 607

• Imbalanced Nutrition: Less Than Body Requirements, related to lack of exogenous nutrients or increased metabolic demand, p. 593

• Disturbed Body Image, related to actual change in body structure, function, or appearance, p. 586

Acute Liver Failure