Esophageal Varices - Hepatic Dysfunction

ESOPHAGEAL VARICES

Bleeding or hemorrhage from esophageal varices occurs in approx-imately one third of patients with cirrhosis and varices. The mor-tality rate resulting from the first bleeding episode is 45% to 50%; it is one of the major causes of death in patients with cirrhosis (Pomier-Layrargues, Villeneuve, Deschenes et al., 2001). The mor-tality rate increases with each subsequent bleeding episode.

Pathophysiology

Esophageal varices are dilated, tortuous veins usually found in the submucosa of the lower esophagus, but they may develop higher in the esophagus or extend into the stomach. This condition nearly always is caused by portal hypertension, which in turn is due to ob-struction of the portal venous circulation within the damaged liver.

Because of increased obstruction of the portal vein, venous blood from the intestinal tract and spleen seeks an outlet through collateral circulation (new pathways of return to the right atrium). The effect is increased pressure, particularly in the vessels in the submucosal layer of the lower esophagus and upper part of the stomach. These collateral vessels are not very elastic but rather are tortuous and fragile and bleed easily (Fig. 39-6). Less common causes of varices are abnormalities of the circulation in the splenic vein or superior vena cava and hepatic venothrombosis.

Bleeding esophageal varices are life-threatening and can result in hemorrhagic shock, producing decreased cerebral, hepatic, and renal perfusion. In turn, there is an increased nitrogen load from bleeding into the GI tract and an increased serum ammonia level, increasing the risk for encephalopathy. Usually the dilated veins cause no symptoms unless the portal pressure increases sharply and the mucosa or supporting structures become thin. Then massive hemorrhage takes place.

Factors that contribute to hemorrhage are muscular exertion from lifting heavy objects; straining at stool; sneezing, coughing, or vomiting; esophagitis; irritation of vessels by poorly chewed foods or irritating fluids; or reflux of stomach contents (especially alcohol). Salicylates and any medication that erodes the esophageal mucosa or interferes with cell replication also may contribute to bleeding.

Clinical Manifestations

The patient with bleeding esophageal varices may present with hematemesis, melena, or general deterioration in mental or phys-ical status and often has a history of alcohol abuse. Signs and symptoms of shock (cool clammy skin, hypotension, tachycardia) may be present.

Assessment and Diagnostic Findings

Endoscopy is used to identify the bleeding site, along with barium swallow, ultrasonography, CT, and angiography.

ENDOSCOPY

Immediate endoscopy is indicated to identify the cause and the site of bleeding; at least 30% of patients suspected of bleeding from esophageal varices bleed from other sources (gastritis, ulcers). Nursing support can be effective in relieving anxiety during this often-stressful experience. Careful monitoring can detect early signs of cardiac dysrhythmias, perforation, and hemorrhage.

After the examination, fluids are not given until the gag reflex returns. Lozenges and gargles may be used to relieve throat dis-comfort if the patient’s physical condition and mental status per-mit. If the patient is actively bleeding, oral intake will not be permitted and the patient will be prepared for further diagnostic and therapeutic procedures.

PORTAL HYPERTENSION MEASUREMENTS

Portal hypertension may be suspected if dilated abdominal veins and hemorrhoids are detected. A palpable enlarged spleen (splenomegaly) and ascites may also be present. Portal venous pressure can be measured directly or indirectly. Indirect mea-surement of the hepatic vein pressure gradient is the most com-mon procedure; it requires insertion of a fluid-filled balloon catheter into the antecubital or femoral vein. The catheter is ad-vanced under fluoroscopy to a hepatic vein. A “wedged” pressure (similar to pulmonary artery wedge pressure) is obtained by oc-cluding the blood flow in the blood vessel; pressure in the unoc-cluded vessel is also measured. Although the values obtained may underestimate portal pressure, this measurement may be ob-tained several times to evaluate the results of therapy.

Direct measurement of portal vein pressure can be obtained by several methods. During laparotomy, a needle may be intro-duced into the spleen; a manometer reading of more than 20 mL saline is abnormal. Another direct measurement requires inser-tion of a catheter into the portal vein or one of its branches. En-doscopic measurement of pressure within varices is used only in conjunction with endoscopic sclerotherapy.

LABORATORY TESTS

Laboratory tests may include various liver function tests, such as serum aminotransferase, bilirubin, alkaline phosphatase, and serum proteins. Splenoportography, which involves serial or segmental x-rays, is used to detect extensive collateral circulation in esoph-ageal vessels, which would indicate varices. Other tests are hepato-portography and celiac angiography. These are usually performed in the operating room or radiology department.

Medical Management

Bleeding from esophageal varices can quickly lead to hemor-rhagic shock and is an emergency. This patient is critically ill, requiring aggressive medical care and expert nursing care, and is usually transferred to the intensive care unit for close moni-toring and management.

The extent of bleeding is evaluated and vital signs are monitored continuously when hematemesis and melena are present. Signs of potential hypovolemia are noted, such as cold clammy skin, tachy-cardia, a drop in blood pressure, decreased urine output, restless-ness, and weak peripheral pulses. Blood volume is monitored by a central venous pressure or arterial catheter. Oxygen is administered to prevent hypoxia and to maintain adequate blood oxygenation.

Because patients with bleeding esophageal varices have intra-vascular volume depletion and are subject to electrolyte imbal-ance, intravenous fluids with electrolytes and volume expanders are provided to restore fluid volume and replace electrolytes. Trans-fusion of blood components also may be required. An indwelling urinary catheter is usually inserted to permit frequent monitoring of urine output.

A variety of pharmacologic, endoscopic, and surgical approaches are used to treat bleeding esophageal varices, but none is ideal and most are associated with considerable risk to the patient. Non-surgical treatment of bleeding esophageal varices is preferable be-cause of the high mortality rate of emergency surgery for control of bleeding esophageal varices and because of the poor physical condition of the patient with severe liver dysfunction.

PHARMACOLOGIC THERAPY

In an actively bleeding patient, medications are administered ini-tially because they can be obtained and administered quickly; other therapies take longer to initiate. Vasopressin (Pitressin) may be the initial mode of therapy because it produces constriction of the splanchnic arterial bed and a resulting decrease in portal pressure. It may be administered intravenously or by intra-arterial infusion (Menon & Kamath, 2000). Either method requires close moni-toring by the nurse. Vital signs and the presence or absence of blood in the gastric aspirate indicate the effectiveness of vasopressin. Monitoring of fluid intake and output and electrolyte levels is nec-essary because hyponatremia may occur and vasopressin may have an antidiuretic effect. Coronary artery disease is a contraindication to the use of vasopressin, because coronary vasoconstriction is a side effect that may precipitate myocardial infarction.

The combination of vasopressin and nitroglycerin (adminis-tered by the intravenous, sublingual, or transdermal route) has been effective in reducing or preventing the side effects (constriction of coronary vessels and angina) caused by vasopressin alone.

Somatostatin and octreotide (Sandostatin) have been reported to be more effective than vasopressin in decreasing bleeding from esophageal varices without the vasoconstrictive effects of vaso-pressin. These medications cause selective splanchnic vasoconstric-tion. Propranolol (Inderal) and nadolol (Corgard), beta-blocking agents that decrease portal pressure, have been shown to prevent bleeding from esophageal varices in some patients; however, it is recommended that they be used only in combination with other treatment modalities such as sclerotherapy, variceal banding, or balloon tamponade. Nitrates such as isosorbide (Isordil) lower por-tal pressure by venodilation and decreased cardiac output. Further studies of these and other medications are necessary to evaluate their use in the treatment and prevention of bleeding episodes.

BALLOON TAMPONADE

To control hemorrhage in certain patients, balloon tamponade may be used. In this procedure, pressure is exerted on the cardia (upper orifice of the stomach) and against the bleeding varices by a double-balloon tamponade (Sengstaken-Blakemore tube) (Fig. 39-7). The tube has four openings, each with a specific pur-pose: gastric aspiration, esophageal aspiration, inflation of the gastric balloon, and inflation of the esophageal balloon.

The balloon in the stomach is inflated with 100 to 200 mL of air. An x-ray confirms proper positioning of the gastric balloon. Then the tube is pulled gently to exert a force against the gastric cardia. 

Traction may be applied with weights or by attachment to a football helmet. Irrigation of the tubing is performed to de-tect bleeding; if returns are clear, the esophageal balloon is not in-flated. If bleeding continues, the esophageal balloon is inflated. The desired pressure in the esophageal and gastric balloons is 25 to 40 mm Hg, as measured by the manometer. There is a possi-bility of injury or rupture of the esophagus with inflation of the esophageal balloon, so constant nursing surveillance is necessary.

Gastric suction is provided by connecting the gastric catheter outlet to suction. The tubing is irrigated hourly, and drainage will indicate whether bleeding has been controlled. Room-temperature lavage or irrigation may be used in the gastric balloon. The pressure within the esophageal balloon is measured and recorded every 2 to 4 hours via the manometer to detect underinflation or over-inflation with potential for esophageal injury. When it appears that bleeding has stopped, the balloons are carefully and sequentially deflated. The esophageal balloon is deflated first and the patient is monitored for recurrent bleeding. After several hours without bleeding, the gastric balloon may be deflated safely. If there is still no bleeding, the tamponade tube is removed. The therapy is used for as short a time as possible to control bleeding while emergency treatment is completed and definitive therapies are instituted (no longer than 24 hours).

Although balloon tamponade has been fairly successful, there are some inherent dangers. Displacement of the tube and the in-flated balloon into the oropharynx can cause life-threatening ob-struction of the airway and asphyxiation. This may occur if a patient pulls on the tube because of confusion or discomfort. It may also result from rupture of the gastric balloon, allowing the esophageal balloon to move into the oropharynx. Sudden rupture of the balloon causes airway obstruction and aspiration of gastric contents into the lungs. The tube is tested before insertion to minimize this risk. Aspiration of blood and secretions into the lungs is frequently associated with balloon tamponade, especially in the stuporous or comatose patient. Endotracheal intubation before insertion of the tube protects the airway and minimizes the risk of aspiration. Ulceration and necrosis of the nose, the mu-cosa of the stomach, or the esophagus may occur if the tube is left in place or inflated too long or at too high a pressure.

These potential complications necessitate intensive and expert care. A confused or restless patient with this tube in place and bal-loons inflated requires close monitoring to prevent its displacement. Nursing measures include frequent mouth and nasal care. For se-cretions that accumulate in the mouth, tissues should be within easy reach of the patient. Oral suction may be necessary to re-move oral secretions. Because of the many potential complications, balloon tamponade tubes are used only as a temporary measure.

The patient with esophageal hemorrhage is usually extremely anxious and frightened. Knowing that the nurse is nearby and will respond immediately can help alleviate some of this anxiety. Tube insertion is uncomfortable and never pleasant. Explana-tions during the procedure and while the tube is in place may be reassuring to the patient.

Although the use of balloon tamponade stops the bleeding in 90% of patients, bleeding recurs in 60% to 70%, necessitating other treatment modalities (eg, sclerotherapy or banding) (Menon Kamath, 2000). Once the balloons are deflated or the tube is re-moved, the patient must be assessed frequently because of the high risk for recurrent bleeding.

ENDOSCOPIC SCLEROTHERAPY

In endoscopic sclerotherapy (Fig. 39-8) (also referred to as injec-tion sclerotherapy), a sclerosing agent is injected through a fiberop-tic endoscope into the bleeding esophageal varices to promote thrombosis and eventual sclerosis. The procedure has been used suc-cessfully to treat acute GI hemorrhage (Menon & Kamath, 2000; O’Grady et al., 2000). Endoscopic variceal sclerotherapy has been used in the primary prophylaxis of variceal bleeding, but the results are poorer than those of pharmacotherapy (Sarin, Lamba, Kumar et al., 1999).

After treatment, the patient must be observed for bleeding, per-foration of the esophagus, aspiration pneumonia, and esophageal stricture. Antacids may be administered after the procedure to counteract the effects of peptic reflux.

ESOPHAGEAL BANDING THERAPY (VARICEAL BAND LIGATION)

In variceal banding (Fig. 39-9), a modified endoscope loaded with an elastic rubber band is passed through an overtube directly onto the varix (or varices) to be banded. After suctioning the bleeding varix into the tip of the endoscope, the rubber band is slipped over the tissue, causing necrosis, ulceration, and eventual sloughing of the varix.

Variceal banding is comparable to endoscopic sclerotherapy in the effective control of bleeding. Compared with sclerotherapy, variceal banding also significantly reduces rebleeding rates, mortal-ity, procedure-related complications, and the number of sessions needed to eradicate varices. Complications include superficial ul-ceration and dysphagia, transient chest discomfort, and rarely esophageal strictures (Menon & Kamath, 2000). Recently, en-doscopic variceal band ligation has been shown to be safe and more effective than propanolol for preventing a first bleeding episode (Sarin et al., 1999).

TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNTING

Transjugular intrahepatic portosystemic shunting (TIPS) is a method of treating esophageal varices in which a cannula is threaded into the portal vein by the transjugular route. An expandable stent is inserted and serves as an intrahepatic shunt between the portal circulation and the hepatic vein (Fig. 39-10), reducing portal hypertension.

Creation of a TIPS is indicated for the treatment of recurrent variceal bleeding refractory to pharmacologic or endoscopic ther-apy. It has also been indicated for the control of refractory ascites. This technique is also used as a bridge to liver transplantation. Complications may include bleeding, sepsis, heart failure, organ perforation, shunt thrombosis, and progressive liver failure (Pomier-Layrargues et al., 2001).

SURGICAL MANAGEMENT

Several surgical procedures have been developed to treat esophageal varices and to minimize rebleeding, but they are often accompa-nied by significant risk. Procedures that may be used for esophageal varices are direct surgical ligation of varices; splenorenal, meso-caval, and portacaval venous shunts to relieve portal pressure; and esophageal transection with devascularization. Use of these pro-cedures is controversial, and studies regarding their effectiveness and outcomes are ongoing (Bacon & Di Bisceglie, 2000).

Surgical Bypass Procedures.

Surgical decompression of the por-tal circulation can prevent variceal bleeding if the shunt remains patent (Bacon & Di Bisceglie, 2000). One of the various surgical shunting procedures (Fig. 39-11) is the distal splenorenal shunt made between the splenic vein and the left renal vein after splenectomy. A mesocaval shunt is created by anastomosing the superior mesenteric vein to the proximal end of the vena cava or to the side of the vena cava using grafting material. The goal of distal splenorenal and mesocaval shunts is to drain only a portion of venous blood from the portal bed to decrease portal pressure; thus, they are considered selective shunts. The liver continues to receive some portal flow, and the incidence of encephalopathy may be reduced. Portacaval shunts divert all portal flow to the vena cava via end-to-side or side-to-side approaches, so they are considered nonselective shunts.

These procedures are extensive and are not always successful be-cause of secondary thrombosis in the veins used for the shunt as well as complications (eg, encephalopathy, accelerated liver failure). The efficacy of these procedures has been studied extensively. The most recent studies have found that all shunts are equally effective in preventing recurrent variceal bleeding but may cause further im-pairment of liver function and encephalopathy. Partial portacaval shunts with interposition grafts are as effective as other shunts but are associated with a lower rate of encephalopathy (de Franchis, 2000; Krige & Beckingham, 2001; Orozco & Mercado, 2000). 

The severity of the disease (by Child’s classification) and the potential for future liver transplantation guide the physician’s choice of intervention. If the cause of portal hypertension is the rare Budd-Chiari syndrome or other venous obstructive disease, aportacaval or a mesoatrial shunt may be performed (see Fig. 39-11). The mesoatrial shunt is required when the infrahepatic vena cava is thrombosed and must be bypassed.

Devascularization and Transection.

Devascularization and staple-gun transection procedures to separate the bleeding site from the high-pressure portal system have been used in the emergency management of variceal bleeding. The lower end of the esopha-gus is reached through a small gastrostomy incision; a staple gun permits anastomosis of the transected ends of the esophagus. Re-bleeding is a risk, and the outcomes of these procedures vary among patient populations.

Nursing Management

Overall nursing assessment includes monitoring the patient’s phys-ical condition and evaluating emotional responses and cognitive sta-tus. The nurse monitors and records vital signs and assesses the patient’s nutritional and neurologic status. This assessment will as-sist in identifying hepatic encephalopathy resulting from the break-down of blood in the GI tract and a rising serum ammonia level. Manifestations range from drowsiness to encephalopathy and coma.

Complete rest of the esophagus may be indicated with bleed-ing, so parenteral nutrition is initiated. Gastric suction usually is initiated to keep the stomach as empty as possible and to prevent straining and vomiting. The patient often complains of severe thirst, which may be relieved by frequent oral hygiene and moist sponges to the lips. The nurse closely monitors the blood pres-sure. Vitamin K therapy and multiple blood transfusions often are indicated because of blood loss. A quiet environment and calm reassurance may help to relieve the patient’s anxiety and reduce agitation.

Bleeding anywhere in the body is anxiety-provoking, resulting in a crisis for the patient and family. If the patient has been a heavy user of alcohol, delirium secondary to alcohol withdrawal can complicate the situation. The nurse provides support and ex-planations regarding medical and nursing interventions. Moni-toring the patient closely will help in detecting and managing complications.Management modalities and nursing care of the patient with bleeding esophageal varices are summarized in Table 39-2.