PATHOPHYSIOLOGICAL MECHANISMS
Portal hypertension is the primary cause of esophageal varices. Blood flow through the liver is diminished, which increases blood flow through the microscopic blood vessels in the esophageal wall. As the blood flow increases, the blood vessels begin to dilate. This dilation can be profound.
The blood vessels continue to dilate until they become large enough to rupture. Rupture of esophageal varices rapidly becomes an emergency situation. The mortality rate associated with rupture is high. Treatment of the esophageal varices is first directed toward immediately controlling the bleeding, then toward long-term medical therapy. Immediate control of the bleeding usually is accomplished endoscopically. The goal of medical management and long-term therapy is to reduce the risk of bleeding.
Patients with cirrhosis have a disorganization of hepatic tissues that is caused by fibrosis and nodular regeneration. The changes in liver structure lead to an increase in the portal venous pressure (i.e., portal hypertension) (Chambers, 2001). New vascular channels may develop and form shunts. As a result, venous blood in the splanchnic system may be diverted from the liver to the systemic circulation through the development of connections to neighboring low-pressure veins. These connections are known as collateral circulation (Chambers, 2001).
The normal portal venous pressure is 2 to 6 mm Hg. Obstruction of the portal venous system leads to increased portal pressure. An elevated portal venous pressure distends the veins proximal to the site of the blockage. This distention increases the capillary pressure in organs drained by the obstructed veins. As the pressure in these veins increases, they become distended with blood, the vessels enlarge, and varices develop. For varices to form, the portal venous pressure must exceed 10 mm Hg (Chambers, 2001).
Rupture of esophageal varices, which is often painless, results in hemorrhage with hematemesis and/or bloody stools. Rupture is caused by a combination of elevated portal venous pressure and erosion of varices by gastric acid.
EPIDEMIOLOGY AND ETIOLOGY
Research data on the outcome in patients with hemorrhagic esophageal varices are grim; a large percentage of these patients either die or suffer from rebleeding. However, according to the Hospital Discharge Register and the Causes of Death Register (Stokkeland et al., 2006), patient outcomes over the past 35 years have improved. The 5-year survival rate in men younger than 50 years of age has increased from 31% to 49%. The mortality rate for esophageal variceal bleeding, on the first event, is 40% to 70%. Huether (2002) found that, “Mortality from ruptured esophageal varices in general ranges from 30% to 60%.”Mortality is related to a number of factors, including liver failure, sepsis, exsanguination, and cerebral edema.
Research has shown that a combination of better treatment regimens and prophylactic treatment options has improved the mortality rate in esophageal variceal hemorrhage. (Herrine, 2005). According to Wu and Chan (2005), both the rebleeding and mortality rates of variceal hemorrhage have been reduced significantly as a result of advances in endoscopic therapy and the use of vasoactive agents. These researchers also credit the use of antibiotic prophylaxis and portasystemic shunts for the decline in the mortality rate (Wu & Chan, 2005).
Not only are esophageal varices associated with a high mortality rate, they also are associated with high health care costs. Both beta blockers and endoscopic procedures have proven to be effective treatment methods, but early detection is still crucial to reducing the risk of hemorrhage, morbidity, and mortality (Suzuki et al., 2005).
Esophageal varices are associated with a higher mortality rate than any other symptom of portal hypertension, and cirrhosis is the most common cause of portal hypertension, accounting for 84% of all cases (Oura et al., 1994).
RISK PROFILE
The populations at greatest risk for the development of esophageal varices are individuals who tend to have a history of chronic cirrhosis, liver cancer, or metastasis. Determinants of the risk of developing esophageal varices include:
• Alcohol-induced cirrhosis
• Hepatocellular carcinoma or cancer metastatic to the liver
• Portal venous pressure greater than 10 mm Hg
• Liver failure
• Liver-associated ascites
• Aortopexy (superior vena cava syndrome) in children
• Use of protease inhibitors
• Ovarian cancer
• Esophageal cancer
• Cholangiocarcinoma, Klatskin’s tumors
• History of esophageal varices or previous bleed (Sidhu & Wilbur, 2005)
• Increased portal pressure with longitudinal red streaks or spots or diffuse erythema seen during endoscopy (Sidhu & Wilbur, 2005)
• Larger varices pose a greater risk of hemorrhage (Sidhu & Wilbur, 2005).
• Laboratory abnormalities include increased bilirubin and elevated liver function tests.
• Patients at risk for rebleeding of an esophageal varix include:
• Those with a history of alcoholism
• The elderly and patients who suffered shock episodes during the initial hemorrhage
• Patients with multiple co-morbidities, especially liver cancer and cirrhosis
• Patients with a bleeding coagulopathy
PROGNOSIS
If esophageal varices are left untreated, the prognosis is poor, and death could occur by profound hemorrhage or airway obstruction. Esophageal variceal bleeding can resolve spontaneously, but early treatment and close monitoring are indicated.
After the initial bleeding episode, the patient is at a risk for rebleeding. Huether (2002) found that “Recurrent bleeding indicates a poor prognosis; most patients die within one year.”
PROFESSIONAL ASSESSMENT CRITERIA (PAC)
1. Hematemesis: Vomiting of either bright red or coffee ground-like blood.
2. Signs and symptoms of hemorrhage: Hypotension, tachycardia, dizziness, dyspnea, tachypnea, restlessness, anxiety, decreased level of consciousness, decreased urine output, and cool, clammy skin.
3. Signs and symptoms of shock: Hypotension, decreased cardiac output, bradycardia.
4. Signs and symptoms of liver failure: Jaundice, ascites, splenomegaly, venous hums, weakness, malaise, anorexia, nausea and vomiting, weight loss, abdominal pain, edema, dark urine, encephalopathy.
5. The Child-Pugh classification (sometimes called the Child-Turcotte-Pugh Score) is used to assess chronic liver cirrhosis, to determine the prognosis and treatment options, and to evaluate the patient for liver transplantation. The score uses five clinical measures of liver disease. Each measure is assigned 1 to 3 points, with 3 representing the severest condition (Table 14-1).
| Parameter | 1 Point | 2 Points | 3 Points |
|---|---|---|---|
| Bilirubin (total) | <34 mcgmol/L (<2 mg/dL) | 34-50 mcgmol/L (2-3 mg/dL) | >50 mcgmol/L (>3 mg/dL) |
| Serum albumin | >35 mg/L | 28-35 mg/L | <28 mg/L |
| INR | <1.7 | 1.71-2.20 | > 2.20 |
| Ascites | None | Suppressed with medication | Refractory |
| Hepatic encephalopathy | None | Grade I or II (or suppressed with medication) | Grade III or IV (or refractory) |
| Prognosis for Liver Disease Based on the Total Score | |||
| Points | Class | Life Expectancy | Perioperative Mortality |
| 5-6 | A | 15-20 months | 10% |
| 7-9 | B | Candidate for transplantation | 30% |
| 10-15 | C | 1-3 months | 82% |
NURSING CARE AND TREATMENT
The treatment of esophageal varices is a collaborative effort that includes nursing assessment and interventions, pharmacologic therapy, and interventional procedures or surgery. Once esophageal varices rupture and begin to hemorrhage, medical treatment becomes an emergent situation requiring immediate care.
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1. Rupture of esophageal varices requires the following interventions:
• Maintain an open airway, position the patient to enhance breathing and expulsion of hematemesis, and suction excess secretions and blood.
• Assess the rate and volume of bleeding. Assess blood pressure and pulse with the patient in the supine position and in the sitting position.
• Insert an IV access and administer fluids and blood products, rapid infusion of 5% dextrose, and a colloid solution until blood pressure is restored and urine output is adequate.
• Correct clotting factor deficiencies with fresh frozen plasma, fresh blood, and vitamin K1.
• Insert a nasogastric tube to assess the severity of bleeding and to lavage gastric contents before endoscopy.
• Prepare for pharmacologic therapy (octreotide or somatostatin) and endoscopy as soon as the patient has been resuscitated. The aim is to establish the cause and to control the bleeding.
2. In nonemergency situations, determine whether the patient is hemodynamically stable or unstable.
3. Assess for coughing and choking and maintain the airway.
4. Infuse IV fluid replacement with isotonic fluids (avoid lactate solutions) and monitor response to fluid replacement.
5. Replace clotting factors.
6. Prepare for possible procedures such as endoscopic variceal sclerotherapy.
7. Assess for signs of slow bleeding and anemia.
8. Hallmark signs and symptoms of bleeding include coughing or choking; cool, dusky skin; and altered mentation.
9. Monitor vital signs for rapid pulse, high blood pressure initially (due to vasoconstrictive compensatory response, then may become low), tachypnea, low central venous pressure, low pulmonary artery pressure, low to normal temperature.
10. Assess for other co-morbidities and medical history.
11. Significant laboratory values:
• Low hemoglobin and hematocrit
• Elevated INR (prolonged PT)
• Decreased platelets
• Elevated WBC
• Hyperkalemia
• Hypernatremia
• Elevated BUN and creatinine
• Elevated ammonia
• Elevated lactate
• Elevated liver function tests (high alanine aminotransferase [ALT], high aspartate aminotransferase [AST])
• ABGs (metabolic acidosis)
• Occult blood in stool
• High urine specific gravity
12. Pharmacologic therapy:
• Patients with esophageal varices and no prior history of variceal hemorrhage should be treated with nonselective beta-adrenergic blockers (e.g., propranolol, nadolol, timolol), provided that the use of beta blockers is not contraindicated. Garcia-Tsao (2006) found that, “Therapy with nonselective beta blockers is the gold standard in the prevention of first variceal hemorrhage in patients with medium to large varices and has been compared to endoscopic variceal ligation in several randomized trials.” Beta blocker therapy has proven to reduce the risk of first bleeding in patients with evidence of varices and recurrent bleeding and mortality in patients with a history of previous variceal hemorrhage. Beta blockers lower portal hypertension by reducing cardiac output, which leads to splanchnic vasoconstriction and a reduction in portal pressures. Beta blockers reduce the risk of recurrent bleeding by 34% and mortality by 26% (Wilbur & Sidhu, 2005).
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