About half of patients with bleeding esophageal varices die. This high death rate reflects not only the massive hemorrhage but also the frequent presence of severely compromised liver function and other systemic disease that may be related to alcohol abuse. Malnutrition, pulmonary aspiration and infection, coronary artery disease are frequent coexisting conditions. Additional complicating factors in this population include lack of cooperation with treatment and acute alcohol withdrawal, which in its worst manifestation (delirium tremens) adds greatly to the already high mortality rate.
Symptoms and Signs of Bleeding Esophageal Varices
The initial management of massive gastrointestinal hemorrhage must be emphasized that bleeding from varices cannot be accurately diagnosed on clinical grounds. Most patients with bleeding esophageal varices have alcoholic cirrhosis, the diagnosis may seem obvious in a patients with hepatomegaly, jaundice, and vascular spiders who admits to recent binge drinking. Splenomegaly, the most constant physical finding, is present in 80% of patients. Ascites is frequently present. Massive ascites and hepatosplenomegaly in a nonalcoholic would suggest the much less common Budd-Chiari syndrome. If cirrhosis or varices have been documented on previous examinations, hematemesis would strongly suggest bleeding varices as the cause.
Most patients with bleeding esophageal varices have compromised liver function. The bilirubin is usually elevated, and the serum albumin is often below 3 g/dL. The leukocyte count may be elevated. Anemia may be a reflection of alcoholic liver disease or hypersplenism as well as acute hemorrhage. The development of a hepatoma by a cirrhotic may first manifested by hemorrhage from varices; CT scan and determination of serum alpha-fetoprotein will make the diagnosis. Thrombocytopenia and coagulopathy are common.
Emergency esophagogastroscopy is the most useful procedure for diagnosing bleeding varices, it should be scheduled as soon the general condition is stabilized by blood transfusion and other supportive measures. Endotracheal intubation may be necessary for airway control. Varices appear as three or four large, tortuous submucosal bluish vessels running longitudinally in the esophagus. The bleeding site may be identified, but in some cases the lumen fills with blood so rapidly that the lesion is obscured.
Upper Gastrointestinal Series
A barium swallow outlines the varices in about 90% of affected patients, but barium studies are neither as sensitive nor as specific as endoscopy, and they are difficult and dangerous in the bleeding patient.
Treatment of Acute Bleeding
The general goal of treatment of bleeding esophageal varices is to control the bleeding as quickly and reliably as possible using methods with the fewest possible side effects.
The patient’s condition is stabilized to the extent possible by following the general guidelines for treating major upper gastrointestinal bleeding. Other therapy should include measures to treat or prevent encephalopathy, parenteral vitamin K to correct a prolonged prothrombin time, and electrolyte replacement (especially potassium) as required to restore electrolyte balance.
Endoscopic sclerotherapy or banding is the initial therapy of choice. Vasopressin or propranolol may be included in the initial resuscitative regimen. Balloon tamponade is no longer used routinely but is rather reserved for special situations when other methods fail.
These measures are successful in approximately 90% of cases, but the early rebleeding rate is about 30%. When bleeding continues after initial treatment, if the patient is a good operative risk, an emergency shunt procedure should be considered.
Death rates rise rapidly in patients requiring more than ten units of blood, in general, patients still bleeding after six units—or those whose bleeding is still unchecked 24 hours after admission — should be considered for portal decompression procedures. Even when the bleeding is brought under control by the initial intervention, the mortality rate remains high (about 35%) as a result of liver failure.
Acute Endoscopic Sclerotherapy or Ligation
Via fiberoptic endoscopy, 1–3 mL of sclerosant solution is injected into the lumen of each varix, causing it to become thrombosed. Variations in the type of endoscope or sclerosant solution or whether or not the varices are physically compressed, etc, appear to have little influence on the outcome. Endoscopy is usually repeated within 48 hours and then once or twice again at weekly intervals, at which time any residual varices are injected.
Sclerotherapy controls acute bleeding in 80% of patients, and rebleeding during the same hospitalization is about half (25% versus 50%) the rebleeding rate of patients treated with a vasopressin and balloon tamponade. Even though controlled trials show improvement in the control of bleeding with sclerotherapy, the evidence for increased patient survival is conflicting.
A similar effect can be achieved by endoscopic ligation of the varices. The varix necroses to leave a superficial ulcer. A controlled trial has reported rubber band ligation to be effective in controlling bleeding (eg, fewer episodes of rebleeding; lower mortality rate) than sclerotherapy.
Vasopressin and Terlipressin
Vasopressin and terlipressin lower portal blood flow by directly constricting splanchnic arterioles, thereby reducing inflow. Vasopressin alone controls acute bleeding in about 80% of patients, and this increases to 95% when used in conjunction with balloon tamponade. Cardiac output, oxygen delivery to the tissues, hepatic blood flow, and renal blood flow are also decreased — effects that occasionally produce complications such as myocardial infarction, cardiac arrhythmias, and intestinal necrosis.
Although the results are somewhat contradictory, controlled trials generally indicate that vasopressin with nitroglycerin is superior to vasopressin alone and that vasopressin alone is superior to placebo in controlling active variceal bleeding. Survival is not increased, however. Vasopressin is given as a peripheral intravenous infusion (at about 0.4 units/min), which is safer than bolus injections. Nitroglycerin can be given intravenously or sublingually. Terlipressin, a synthetic vasopressin analogue, undergoes gradual conversion to vasopressin in the body and is safe to give by intravenous bolus injection (2 mg intravenously every 6 hours). It may cause fewer cardiac side effects than vasopressin.
Somatostatin and the synthetic longer-lasting analogue octreotide have the same effect on the splanchnic circulation but without significant side effects. Octreotide is given as an initial bolus of 100 g followed by a continuous of 25 /h for 24 hours.
Tubes designed for tamponade have two balloons that can be inflated in the lumen of the gut to compress bleeding varices. There are three or four lumens in the tube, depending on the type: two are for filling balloons within the stomach and the esophagus and the third permits aspiration of gastric contents. A fourth lumen in the Minnesota tube is used to aspirate the esophagus orad to the esophageal balloon. The main effect results from traction applied to the tube, which forces the gastric balloon to compress the collateral veins at the cardia of the stomach. Inflating the esophageal balloon probably contributes little, since barium x-rays suggest that it does not actually compress the varices.
The most common serious complication is aspiration of pharyngeal secretions and pneumonitis.
Another serious hazard is the occasional instance of esophageal rupture caused by inflation of the esophageal balloon. The esophageal balloon is therefore infrequently used.
About 75% of actively bleeding patients can be controlled by balloon tamponade. When bleeding has stopped, the balloons are left inflated for another 24 hours. They are then decompressed, leaving the tube in place. If bleeding does not recur, the tube should be withdrawn.
Surgery of Bleeding Esophageal Varices
The operative procedures to control bleeding esophageal varices are emergency portasystemic shunt and variceal ligation or esophageal transection.
Emergency Portacaval Shunt
An emergency portasystemic shunt has a 95% rate of success in stopping variceal bleeding. The death rate of the operation is related to liver function (eg, Child-Pugh classification) and its effects on cardiac, renal, and pulmonary function. Some patients with liver disease, especially those with severe encephalopathy and ascites, have an extraordinarily poor survival regardless of the treatment. In such patients, surgery is usually not warranted, even in the face of continued bleeding. A controlled trial showed that the death rate in acutely bleeding Child’s C patients was insignificantly lower after endoscopic sclerotherapy (44%) than after emergency portacaval shunt (50%).
For active bleeding, an end-to-side portacaval shunt or H-mesocaval shunt is most commonly performed.
The distal splenorenal (Warren) shunt is usually too time-consuming for use in emergency operations. The central splenorenal shunt is more complicated than an end-to-side portacaval shunt and has no specific advantages.
Renal failure, which is often accompanied by ascites, is another potentially lethal problem. Metabolic alkalosis and delirium tremens are not uncommon postoperatively in alcoholics.
Varices may be obliterated by firing the end-to-end stapler in the distal esophagus after tucking a full-thickness ring of tissue into the cartridge with a circumferential tie. This procedure has gained popularity in the past decade, and in many surgical units it is the first choice for therapy when nonsurgical methods fail. If transection is performed. As a last-ditch effort — after many units of blood have been transfused — death from liver failure is all but certain. The results (eg, survival) are better with nonalcoholic cirrhosis. Stapled transection has replaced the older technique of direct suture ligation of the bleeding esophageal varices. Transection must be viewed as an emergency measure to stop persistent bleeding—not as definitive treatment—since the underlying portal hypertension is not corrected and varices recur months later in many patients.