CHAPTER 9 Gastrointestinal disorders
Gastrointestinal assessment: general
Goal of system assessment
Evaluate for dysfunctional ingestion and digestion of food and elimination of waste products.
Auscultation
Evaluate bowel sounds in each of the quadrants in a systemic fashion.
• Hyperactive bowel sounds—may indicate diarrhea or early intestinal obstruction
• Hypoactive to absent bowel sounds—may indicate paralytic ileus or peritonitis
• High-pitched rushing sounds—may indicate intestinal obstruction
Evaluate for systolic bruits (humming, swishing, or blowing sounds) over:
If the abdomen is rigid, do not palpate; it is a sign of peritoneal inflammation. Palpation could cause rupture of the inflamed organ.Nutritional assessment
Evaluate for risk factors and indications of malnutrition for which critically ill patients are at risk. Malnutrition may occur due to negative caloric intake with concomitant GI obstruction, malabsorption syndromes, infectious diseases, certain medications, and surgical treatment. Additionally, caloric needs are greatly increased in the critically ill as a result of hypermetabolic states produced by trauma, fever, sepsis, and wound healing.
| Body System | Signs | Deficiency |
|---|---|---|
| Skin, nails | Dry skin Brittle nails; spooned-shaped nails |
Vitamin deficiency Iron deficiency |
| Mouth | Cracks; beefy, red tongue | Vitamin deficiency |
| Stomach | Decreased gastric acidity Delayed gastric emptying |
Protein deficiency |
| Intestines | Decreased motility and absorption Diarrhea |
Protein deficiency Altered normal flora |
| Liver/biliary | Hepatomegaly Ascites |
Decreased absorption of fat-soluble vitamins, Protein deficiency |
| Cardiovascular | Edema Tachycardia; hypotension |
Protein deficiency Fluid volume deficiency |
| Musculoskeletal | Decreased muscle mass Subcutaneous tissue loss |
Protein, carbohydrate, and fat deficiency |
Acute gastrointestinal bleeding
Pathophysiology
Upper gastrointestinal bleeding
The most common cause of hematemesis and melena is gastroduodenal ulcer disease, accounting for half of massive UGI bleeding (UGIB) disorders. Peptic ulcers are chronic, usually solitary, lesions that are most prevalent in the stomach and duodenum. These lesions breach the protective mucosa of the GI tract extending deep into the submucosa, exposing tissue to gastric acids with eventual autodigestion. Bleeding occurs when the ulcer erodes into a blood vessel. Helicobacter pylori (H. pylori) is strongly associated with the pathogenesis of peptic ulceration, much more so than gastric hyperacidity. The toxins and enzymes released by the H. pylori organism are believed to cause ulceration through proinflammatory processes and by decreasing duodenal mucosal bicarbonate production. Infection with H. pylori is present in almost all patients with duodenal ulcers and 70% of patients with gastric ulcers. In contrast, hyperacidity is present in a minority of patients with gastric ulcers and even less in those with duodenal ulcers. Bleeding occurs in 10% to 20% of patients with peptic ulceration, and perforation occurs in about 5%. Another cause of peptic ulceration is Zöllinger-Ellison Syndrome (ZES). In ZES, ulcerations occur in the stomach, duodenum, and jejunum due to excess gastrin secretion by a tumor, resulting in hyperacidity with mucosal erosion. Stress ulceration is a common and potentially life-threatening phenomenon that occurs in critically ill patients, especially those who are mechanically ventilated. Stress ulcers, also known as erosive gastritis, tend to be multiple lesions, located mainly in the stomach and occasionally in the duodenum, primarily resulting from stress-related hyperacidity and mucosal ischemia. Stress ulcers occurring in the proximal duodenum are called Curling ulcers. They are associated with deep mucosal invasion and are seen in patients with major burn injury or major trauma. Cushing ulcer is a related condition occurring in patients who have sustained serious head injury, major surgery, or critical central nervous system (CNS) disorder that raises intracranial pressure. Gastritis, another common cause of peptic ulceration, usually occurs as slow, diffuse oozing that is difficult to control. Benign or malignant gastric tumors may initiate severe bleeding episodes, especially tumors located in the vascular system that supplies the GI tract.
Neighboring organs
Acute pancreatitis (see p. 762) and pancreatic pseudocyst are disorders associated with hemorrhage. Persons with intra-abdominal vascular grafts are at risk for the development of aortoenteric fistulas with massive GI hemorrhage.
Medications
Longstanding use of aspirin, corticosteroids, or anticoagulants is associated with serious GI bleeding. Ethanol may cause or potentiate ulcer bleeding as it induces gastric mucosal injury. Nonsteroidal anti-inflammatory drugs (NSAIDs) cause increased risk of serious GI bleeding, ulceration, and perforation of the stomach and intestines. Traditional NSAIDs are nonselective inhibitors of both cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) enzymes. COX-1 enzymes regulate gastroduodenal mucosal protective mechanisms. COX-2 enzymes are involved in inflammatory and pain responses. The newer COX-2 selective inhibitors were believed to block pain and inflammation while leaving protective mucosal mechanisms intact, thereby significantly lowering the incidence of GI ulceration and bleeding compared with 
traditional NSAIDs. However, the COX-2 inhibitors were shown to increase the risk of cardiovascular disease, especially in older adults, resulting in the removal of two of three COX-2 agents from the market. Currently, celecoxib is the only COX-2 selective inhibitor available in the United States. This COX-2 inhibitor is still associated with an increased risk for GI bleeding, while to a lesser degree than traditional NSAIDS; additionally, it does not appear to pose any greater risk for cardiovascular disease than traditional NSAIDs.
Gastrointestinal assessment: acute gastrointestinal bleeding
Goal of assessment
Evaluate patients for severity of active bleeding, shock states, or risk of rebleeding.
History and risk factors
History and risk factors include critical illness, especially that caused by major injury, surgery, CNS disorder, or burns; prolonged shock or hypoperfusion; organ failure; esophageal varices, excessive alcohol, NSAIDs, or corticosteroid ingestion; inflammatory bowel disease; foreign body ingestion; hiatal hernia; hepatic, pancreatic, or biliary tract disease; blood dyscrasias; penetrating or blunt trauma; familial cancer; recent abdominal surgery; and the presence of H. pylori, found in greater than 90% of patients with duodenal ulcers and 70% of those with gastric ulcers. Identification of those at risk for recurrent bleeding is essential to guide therapy and prevent poor outcomes. Risk factors associated with rebleeding are listed in Box 9-1.
Hematemesis as the initial sign of hemorrhageVital sign assessment
• Systolic BP less than 90 to 100 mm Hg with an HR greater than 100 beats/min (bpm) in a previously normotensive individual signals a 20% or greater reduction in blood volume.
• Orthostatic hypotension signs will be positive revealing a decrease in systolic BP greater than 10 mm Hg with an increase in HR of 10 bpm. Orthostatic hypotension is indicative of recent blood loss of at least 1000 ml in the adult.
• Respiratory rate will be mildly elevated as a response to the diminished oxygen-carrying capacity of the blood. If abdominal pain is present, ventilatory excursion may be limited.
Blood loss
• The amount of blood lost and rate of bleeding will have varying effects on cardiovascular and other body systems.
• Blood loss of 1000 ml within 15 minutes usually produces tachycardia, hypotension, nausea, weakness, and diaphoresis. Adults can lose up to 500 ml of blood in 15 minutes and remain free of associated symptoms.
• Massive hemorrhage, which is generally defined as loss of greater than 25% of total blood volume or a bleeding episode that requires transfusion of 6 units of blood in a 24-hour period, can occur.
• Syncope associated with hypotension also may occur.
• Sequestration of fluid into the peritoneum and interstitium further depletes intravascular volume.
• Severe hypovolemic shock and decreased cardiac output can lead to ischemia of various organs, especially the brain and kidneys.
Abdominal pain
• Mild to severe epigastric pain is often associated with gastroduodenal ulcerative or erosive disease. The pain is described as dull or gnawing.
• As blood covers and protects the eroded tissue, pain may disappear.
• Blood can irritate the bowels, thereby increasing transit time in the lower GI tract, causing diarrhea.
Observation
• Extremities are cool and diaphoretic.
• Pallor or cyanosis may be present.
• Alterations in LOC with restlessness and confusion.
• Emesis or gastric aspirate contains obvious whole blood or old blood that resembles coffee grounds.
• Hematemesis usually occurs with UGIB from above the ligament of Treitz. Bleeding originating below the level of the duodenum is not usually associated with hematemesis.
• Jaundice, vascular spiders, ascites, and hepatosplenomegaly suggest liver disease.
Hemodynamic measurements
• Hypovolemic shock usually reveals a decreased central venous pressure (CVP), pulmonary artery pressure (PAP), central venous oxygen saturation (ScVO2) and cardiac output (CO) and an increased stroke volume variation (SVV) and systemic vascular resistance (SVR).
• After major abdominal surgery, a hyperdynamic state may exist similar to that seen in early septic shock, with an increased CO and decreased SVR (see SIRS, Sepsis and MODS, p. 924).
| Test | Purpose | Abnormal Findings |
|---|---|---|
| Blood Studies | ||
| Complete blood count (CBC) with differential Hemoglobin (Hgb) Hematocrit (Hct) RBC count (RBC) WBC count (WBC) Platelet count |
Serial Hgb and Hct values monitor the amount of blood lost. Total counts monitor hematologic function, except for platelets, which may be nonfunctional despite normal number present. |
Hgb <10 g/dl correlates with increased rebleeding and mortality rates. The first Hct value may be near normal ∼45% because the ratio of blood cells to plasma remains unchanged initially. However, the Hct is expected to fall dramatically ∼27% as volume is restored and extravascular fluid mobilizes into the vascular space (hemodilution). Hct < 24% generally requires transfusion. Platelet count rises within 1 hour of acute hemorrhage. Leukocytosis occurs frequently following acute hemorrhage. |
| Serum chemistry BUN Creatinine BUN:creatinine (Cr) ratio Serum chloride Serum potassium Serum glucose Liver function tests (LFTs): Total bilirubin Ammonia |
To assess fluid and electrolyte status. LFTs monitor for hepatic involvement. | BUN will be elevated due to dehydration. Creatinine may be mildly elevated due to ↓ GFR secondary to hypovolemia. BUN:Cr ratio will be elevated >33:1 mg/dl in the patient with upper GI bleed. Hypochloremia, hypokalemia and ↑serum bicarbonate will be noted with excessive vomiting or gastric suction. Mild hyperglycemia is the result of the body’s compensatory response to a stressful stimulus. Hyperbilirubinemia is caused by the breakdown of reabsorbed RBCs and blood pigments. Ammonia levels are usually elevated in patients with hepatic disease. Plasma protein levels may rise in response to increased hepatic production. |
| Arterial blood gas (ABG) | Assesses acid-base status. Lactic acid levels may be drawn separately, and may be available on certain ABG analyzers. | If the shock state is severe, lactic acidosis occurs, reflected by low arterial pH and serum bicarbonate levels and the presence of an anion gap. With a low perfusion state, hypoxemia may be present. |
| Coagulation studies | Assess for preexisting hypocoagulable disease; liver disease; anticoagulant or antiplatelet therapy for cardiac disease. Large blood volume transfusions may lead to the development of coagulopathies. |
Elevation of fibrinogen levels, fibrin split products (FSP), PT, PTT, INR may be seen. |
| 12-Lead ECG | Monitor for severe cardiac ischemia findings as a result of hypoperfusion. | Ischemic changes include T-wave depression or inversion. |
| Radiologic Procedures | ||
| Esophagogastroduodenoscopy (EGD) | To accurately assess the source of upper GI ulcer bleeding. To locate the ulcer, visualize and implement endoscopic therapy, such as sclerosing bleeding vessels. | Endoscopic ulcer findings (endoscopic stigmata) include: Clean ulcer base Adherent clot Visible vessel Active bleeding |
| Plain films Abdominal radiograph Chest radiograph |
To identify the presence of dilated bowel or free air. A chest x-ray is taken to establish baseline pulmonary status. |
Free air seen under the diaphragm, suggests perforation. |
| Barium studies | Usually are reserved for nonemergent situations to verify the presence of tumors or other large GI lesions. | Not usually used for acute GI bleeding as this procedure does not allow for the provision of endoscopic therapy. |
| Colonoscopy | Direct visualization of the rectum and sigmoid colon through an endoscope for diagnosis and triage of lower GI bleeding. | Mucosal bleeding, polyps, hemorrhoids, and other lesions may be identified. Biopsy specimen may be obtained. Emergent colonoscopy is difficult due to length of time for adequate bowel preparation. |
| Angiography | The visualization of active bleeding from an arterial site or from a large vein in the lower GI tract. Bleeding flow rate must be at least 0.5–1.0 ml/min to be visualized by this test. |
Clearly identifies bleeding GI arterial systems. Therapeutic arterial embolization or vasopressin infusion may be performed to stop the bleeding during angiography. Complications include dye-induced renal failure, arterial dissection and occlusion, bowel infarction, and MI with vasopressin infusion. |
| Nuclear medicine Technetium-labeled red blood cell scan |
To detect low-flow rate bleeding in the lower GI tract. Usefulness is controversial. | Identifies low-flow bleeding rates of 0.1–0.5 ml/min in the lower GI tract. Accuracy remains questionable. |
Esophagogastroduodenoscopy
Esophagogastroduodenoscopy (EGD) is the most accurate means of determining the source of UGI ulcer bleeding. Visualization of the esophagus, stomach, and duodenum using a fiberoptic endoscope passed through the mouth is usually performed within the first 12 hours after the patient’s admission to identify the exact source of bleeding and characteristics of ulcers, if present. Endoscopic ulcer findings are referred to as endoscopic stigmata. Stigmata indicative of bleeding ulcers, bleeding esophageal varices, or ulcers at risk for rebleeding are identified in Box 9-2, Stigmata of Active or Recent Hemorrhage (SARH). SARH findings are helpful in determining the course of direct therapy as well as providing prognostic information. Antacids and sucralfate should be withheld until after the procedure, because they can alter the appearance of lesions. Gastric biopsy is usually obtained with endoscopy for H. pylori diagnosis as well as to exclude gastric malignancy.
Box 9-2 STIGMATA OF ACTIVE OR RECENT HEMORRHAGE (SARH)
Endoscopic ulcer findings from active or recent upper gastrointestinal hemorrhage:
Electrocoagulation, injection therapy (epinephrine), laser, hemoclips, and other therapeutic techniques such as scleral therapy and variceal ligation (banding) may be used during this procedure to stop current bleeding or prevent further bleeding from esophageal varices or ulcers.
Collaborative management
Acute GI bleeding can occur from various lesions or sites in the GI tract. The amount of blood loss can vary from minor to massive (Table 9-2) depending on the cause, resulting in hypovolemic shock with significant associated mortality. The patients requiring intensive care 
management are those with moderate to massive bleeding, advanced age and significant comorbidities such as end-stage renal disease (ESRD), hepatic disease, or cardiovascular disease. Therefore, collaborative management focuses on cessation of active bleeding, identification and treatment of the underlying pathophysiology, and the prevention of rebleeding. Some patients develop GI bleeding during hospitalization for another reason as in the case of stress ulceration. Stress ulcer prophylaxis has been included in the management of mechanically ventilated, critically ill patients but is currently controversial.
| Severity of Bleed | Percent of Intravascular Blood Loss | Blood Pressure (BP) and Heart Rate (HR) Findings |
|---|---|---|
| Massive | 20%–25% | Systolic BP < 90 mm Hg HR >100 beats/min |
| Moderate | 10%–20% | Orthostatic hypotension HR >100 beats/min |
| Minor | <10% | Normal BP HR <100 beats/min |
Adapted from Rockey DC: Gastrointestinal bleeding. In Sleisenger MH, Feldman M, Fordtran JS, et al., editors: Sleisenger & Fordtran’s Gastrointestinal and liver disease: pathophysiology, diagnosis, management, ed 8. Philadelphia, 2006, Saunders.
Care priorities
1. Fluid and electrolyte management:
Volume replacement in acute GI bleeding must be performed as quickly as possible. Large-bore IV lines should be placed and rapid fluid resuscitation initiated. Volume replacement should include a combination of crystalloid and blood products. Unstable patients who show signs of poor tissue perfusion are generally transfused. Packed cells and fresh-frozen plasma should be balanced to provide for both the replacement of cells and clotting components. Large transfusions will cause Ca−+ to bind with the citrate (the preservative in stored blood) and deplete free Ca−+ levels. In addition, large-volume blood transfusions can lead to coagulopathy disorders. Vasopressors and inotropic agents should be used only if tissue perfusion remains compromised despite adequate intravascular volume replacement. Hemodynamic monitoring is essential for continuous evaluation of the patient’s volume status, 
especially in patients older than 50 years or those with chronic illnesses such as cardiovascular, pulmonary, renal, or hepatic disease. Overaggressive volume resuscitation may result in fluid volume excess with complications of cardiac failure and pulmonary edema. Electrolyte levels should be closely monitored, especially in patients with renal or hepatic disease.
hemoglobin remaining. More aggressive ventilatory support may be required for patients with persistent hypoxemia, evidence of early respiratory failure, or impending ARDS, as well as for patients who were overaggressively volume resuscitated.Proton-pump inhibitors deactivate the enzyme system that pumps hydrogen ions from parietal cells thereby inhibiting gastric acid secretion. They have become the preferred agent for erosive ulcer disease with bleeding. Their acid-inhibitory effects are significantly stronger than H2-receptor antagonists. Intravenous (IV) PPIs or high-dose oral PPIs following a bleeding episode are effective in reducing rebleed, the number of transfusions, and the need for further endoscopic therapy.
CARE PLANS FOR ACUTE GASTROINTESTINAL BLEEDING
related to active loss secondary to hemorrhage from the GI tract
Electrolyte and Acid-Base Balance; Fluid Balance
1. Monitor BP every 15 minutes during episodes of rapid, active blood loss or unstable vital signs. Be alert to MAP decreases of greater than 10 mm Hg from previous reading.
2. Monitor postural vital signs on patient’s admission, every 4 to 8 hours, and more frequently if recurrence of active bleeding is suspected: measure BP and HR with patient in a supine position, followed immediately by measurement of BP and HR with patient in a sitting position (as tolerated). A decrease in systolic BP greater than 10 mm Hg or an increase in HR of 10 bpm with patient in a sitting position suggests a significant intravascular volume deficit, with approximately 15% to 20% loss of volume.
3. Monitor HR, ECG, and cardiovascular status hourly, or more frequently in the presence of active bleeding or unstable vital signs. Be alert to a sudden increase in HR, which suggests hypovolemia.
4. Measure central pressures and thermodilution CO every 1 to 4 hours. Be alert to low or decreasing CVP, PAOP, and CO. Calculate SVR every 2 to 4 hours, or more frequently in patients whose condition is unstable. An elevated HR, decreased PAOP, decreased CO (CI less than 2.5 L/min/m2), and increased SVR suggest hypovolemia and the need for volume restoration.
5. Measure urinary output hourly. Be alert to output less than 0.5 ml/kg/hr for 2 consecutive hours. Increase fluid intake or consider fluid bolus if decreased output is caused by hypovolemia and hypoperfusion.
1. Obtain two large-bore IV lines (16- or 18-gauge) and central venous access.
2. Initiate crystalloid replacement therapy with a combination of normal saline and lactated Ringer. Fluid should be warmed to prevent hypothermia.
3. Administer packed red blood cells (PRBCs) for persistently low Hct (less than 20% to 25%). Anticipate Hct will increase by 3% following 1 unit of PRBCs.
4. Fresh-frozen plasma is required after 10 units of packed RBCs is infused.
5. Monitor prothrombin time (PT) and partial thromboplastin time (PTT); administer fresh-frozen plasma (FFP) to maintain normal levels.
6. Monitor ionized calcium levels closely because of calcium’s tendency to bind with citrate. Administer calcium gluconate for ionized calcium levels less than 4.4 mg/dl.
7. Prepare for platelet transfusion if platelets fall below 50,000 or following 10 units of packed RBCs.
1. Initiate fluid replacement (see Fluid and Electrolyte Disturbances, p. 37).
2. Collaborate with physician or midlevel practitioner to administer vasoactive medication if shock persists with volume resuscitation.
3. Monitor for cerebral ischemia or indications of insufficient cerebral blood flow.
4. Monitor renal function (BUN and creatinine levels for elevations) as intravascular volume depletion can lead to prerenal azotemia.
5. Monitor tissue oxygenation using ABG, SvO2, central venous oxygen saturation (ScvO2) monitoring if available, and serum lactate measurements.
6. Monitor ECG for ST-segment depression and T-wave inversion, which may be seen as a result of the shock state.
Bleeding reduction: gastrointestinal
1. Administer proton-pump inhibitors IV at least 3 days in patients whose endoscopic stigmata suggest a high risk of rebleeding. Vasopressin (Pitressin), or Terlipressin (Glypressin) may help slow variceal bleeding.
2. Measure and record all GI blood losses from hematemesis, hematochezia, and melena.
3. Check all stools and gastric contents for occult blood.
4. Ensure proper function and patency of gastric tubes. Do not occlude the air vent of double-lumen tubes, because this may result in vacuum occlusion. Confirm placement of gastric tube at least every 8 hours, and reposition as necessary. Inflated esophageal balloon tubes used for tamponade of varices must be secured and stable.
5. Initiate nasogastric lavage to clear the stomach of blood. Gastric lavage does not slow or stop bleeding as once thought but is necessary prior to endoscopy for optimal visualization.
6. Teach patient signs and symptoms of actual or impending GI hemorrhage: pain, nausea, vomiting of blood, dark stools, lightheadedness, and passage of frank blood in stools. Reinforce the importance of seeking medical attention promptly if signs of bleeding occur.
7. Teach patient the importance of avoiding medications/agents with the potential for gastric irritation: aspirin, NSAIDs, ethanol.
Blood Products Administration; Hemodynamic Regulation; Gastrointestinal Intubation; Bleeding Precautions; Teaching: Individual; Surgical Preparationrelated to decreased preload secondary to acute blood loss
Within 8 hours of this diagnosis, CO approaches normal limits with adequate tissue perfusion as evidenced by CI greater than 2.5 L/min/m2, MAP greater than 70 mm Hg, CVP 2 to 6 mm Hg, urinary output greater than 0.5 ml/kg/hr, normal sinus rhythm on ECG, distal pulses greater than 2+ on a 0 to 4+ scale, and brisk capillary refill (less than 2 seconds).
1. Administer vasopressors and inotropic agents as prescribed if tissue perfusion remains inadequate following intravascular volume replacement.
2. Monitor ECG for evidence of myocardial ischemia (i.e., T-wave depression, QT prolongation, ventricular dysrhythmias).
3. Monitor for physical indicators of diminished cardiac output, including pallor, cool extremities, capillary refill greater than 2 to 3 seconds, and decreased or absent amplitude of distal pulses.
4. Monitor vital signs and CO, and replace volume as indicated (see Fluid and Electrolyte Disturbances, p. 37).
5. Monitor for oliguria hourly; report urine output less than 0.5 ml/kg/hr for 2 consecutive hours.
1. Administer oxygen via nasal cannula or facemask to facilitate maximal oxygen delivery.
2. Monitor pulse oximetry and ABG values for hypoxemia. Report arterial PaO2 less than 80 mm Hg and oxygen saturation below 92%.
3. Prepare for endotracheal intubation and mechanical ventilation if patient is distressed with oxygen saturation less than 90% with supplemental oxygen.
4. Monitor for respiratory crackles, which can result from overaggressive fluid resuscitation.
Cardiac Care: Acute; Oxygen Therapy; Invasive Hemodynamic Monitoring; Dysrhythmia Management
1. Monitor and document presence of abdominal pain or discomfort. Devise a pain scale with patient. Pain may disappear during a bleeding episode since blood covers and protects eroded tissue.
2. Administer gastric alkalizing agents and sucralfate as prescribed to relieve pain caused by upper GI disorders. Hold these agents prior to endoscopy.
3. Measure gastric pH at least every 4 hours. For gastric aspirate, use a clean syringe and discard the first aspirate to ensure accuracy. Some may use nasogastric (NG) tonometer to measure gastric mucosal pH.
4. Adjust gastric alkalizing therapy to maintain pH of 4.0 to 5.0 or other prescribed range. Avoid excessive alkalization, which is associated with increased risk of nosocomial pneumonia.
5. Administer opiate analgesics with caution to hypovolemic patients to avoid hypotension and respiratory depression.
