A client is a candidate for intubation as a result of bleeding esophageal varices

Cirrhosis

Cirrhosis refers to cellular degeneration and fibrotic changes of the liver parenchyma (Fig 1). As a sequela of ESLD, cirrhosis can develop from a multitude of causes that inflict repeated insults to the liver. Alcohol-related and viral insults are the most common causes worldwide.1, 2 In the United States, alcoholic cirrhosis and hepatitis C account for most cases. Other causes for cirrhosis include autoimmune hepatitis, bile duct disorders, nonalcoholic steatohepatitis, and hereditary

Pathophysiology

Chronic elevation of portal venous pressures invariably leads to the development of collateral vessels between portal and systemic circuits.22 These collaterals arise from the opening of pre-existing vessels, through the impaired clearance of vasoactive molecules,22 as well as through angiogenesis.23, 24 Portosystemic collaterals can develop throughout the entire body, including the GI tract, omentum, diaphragm, bladder, and reproductive organs.25 Among these, EVs are the most prevalent in

Classification

Esophageal varices are the most common cause of GI hemorrhage in patients with cirrhosis, accounting for 60%-65% of cases, but a multitude of other etiologies may result in bleeding as well.33 These lesions can be classified into those related to portal hypertension and those seen in the general population (Table 3).71 Portal hypertension–related lesions include EVs, gastric varices, ectopic varices, and portal hypertensive gastropathy. Unrelated lesions include bleeding peptic ulcers, reflux

Resuscitation and stabilization following variceal rupture

If variceal bleeding is suspected, initial measures may include airway protection, hemodynamic monitoring, blood product resuscitation, pharmacologic therapy, and balloon tamponade. These measures are aimed at stabilization of the patient and bridging to definitive diagnosis and therapy (Fig 3).

Endoscopy

Endoscopy is the mainstay of diagnosis and treatment of upper GI tract bleeding for those in whom esophagogastric varices are suspected.102 Emergent endoscopy is recommended and should be completed within the first 12 hours of presentation. Diagnostic endoscopy can become therapeutic if variceal bleeding is confirmed. Endoscopic diagnosis of acute variceal bleeding is made by the confirmation of hemorrhage or stigmata of recent bleeding from varices. Diagnostic endoscopy is also employed to

Endoscopic injection sclerotherapy

Sclerotherapy achieves hemostasis by inducing inflammatory reactions in the variceal lumen and surrounding tissues, leading eventually to mural necrosis and variceal obliteration. Sodium tetradecyl sulfate, morrhuate sodium, ethanolamine, and ethanol have been successfully used as sclerosants.105 Endoscopic injection of tissue adhesives has also been used in conjunction with EIS for gastric fundal varices, which have lower success rates with EIS alone. Some studies have shown that endoscopic

Endoscopic variceal band ligation

Endoscopic band ligation of esophagogastric varices is a newer alternative technique for the management of upper GI tract varices with relatively fewer complications. Endoscopic band ligation of varices avoids the use of sclerosant by mechanically restricting flow into the varix; however, microscopic examination of the treated sites in fact shows ischemic necrosis of the mucosa and submucosa, acute inflammation, and formation of granulation tissue. The technique was first reported by Steigmann.

Adjunct therapies

Endoscopic therapy achieves hemostasis in 90% of patients with acutely bleeding esophagogastric varices; however, the probability of recurrent bleeding may be as high as 50%. Pharmacologic therapy (eg, terlipressin and somatostatin) should be continued for 5 days following endoscopic therapy, and antibiotic prophylaxis is recommended to prevent complications such as spontaneous bacterial peritonitis.102, 112 The continuation of NSBB and nitrates (eg, isosorbide mononitrate) is recommended

Self-expanding stents

New studies suggest that the use of endoscopically placed self-expanding stents may be a safer alternative to balloon tamponade for refractory variceal bleeding.115, 116 Removable, covered, self-expanding metal stents (SEMS) have several advantages over other salvage techniques for difficult variceal bleeding. Deployment of the stent requires fewer resources and can be accomplished without intravenous contrast or fluoroscopy. There is no requirement for endotracheal intubation and oral

Balloon-occluded retrograde transvenous obliteration of gastric varices

Gastric variceal bleeding represents only 20%-30% of all variceal bleeding but presents a unique challenge that often requires a multidisciplinary approach to reliably stop bleeding.118 Acute bleeding from predominantly gastric varices is less amenable to portal decompression using TIPS. Gastric varices related to portal hypertension are often associated with spontaneous formation of gastrorenal or gastrocaval shunts. The development of balloon-occluded retrograde transvenous obliteration

Transjugular intrahepatic portosystemic shunt

For patients who continue to bleed from their varices despite pharmacologic and endoscopic intervention or who experience rebleeding, a portal decompressive procedure is indicated. TIPS has emerged as the first-line treatment for bleeding EVs in this setting. The evolution of TIPS began in the 1960s, when inadvertent access of the portal system occurred during transjugular cholangiography. Following this, animal studies were conducted to explore the use of transhepatic portal access for

Surgical decompression

There are 3 main types of surgical decompression for the treatment of bleeding varices, including surgical shunt creation, liver transplantation, and devascularization procedures. The first account of surgical decompression for portal hypertension was described and performed on animals in the late 1800s by Nikolai Eck for the study of diseases of the liver. The “Eck” fistula is a large side-to-side connection of the portal vein and vena cava (at least 12 mm) with subsequent ligation of the

Totally diverting shunts

Totally diverting shunts completely divert portal flow from the liver by joining the portal vein, or a major branch, to the inferior vena cava or one of its major branches. These include the end-to-side portacaval shunt or “Eck” fistula, large diameter side-to-side portocaval shunt, side-to-side mesocaval shunt, and the central splenorenal shunt. Pressures in the vena cava are significantly lower compared with the portal venous system, creating a reversal or “hepatofugal flow.” This reversal of

Selective surgical shunts

Selective shunts create 2 separate drainage systems, achieving only partial decompression of the portal circulation. Successful selective shunts achieve reduced pressures in the esophagogastric system and higher pressures in the mesenteric system. Portal pressure and flow are maintained, and the risk for postshunt encephalopathy is reduced to between 5% and 14%.153, 154 The 5-year survival rate approaches 80% and cessation of bleeding occurred in nearly 100% of patients.148 Hepatic pressures

Surgical devascularization

Esophageal devascularization is an alternative to shunting in patients with significant portal thrombosis and was introduced by Sugiura and Futagawa.157 This procedure, which later became known as the Sugiura operation, included esophageal transection with extensive paraesophagogastric devascularization, splenectomy, vagotomy, and pyloroplasty via dual transthoracic and transabdominal incisions. Thoracic esophageal exposure is obtained via left lateral thoracotomy at the sixth intercostal

Liver transplantation

Most patients who manifest portal hypertension by variceal bleeding have ESLD. Therapy with liver transplantation offers the most definitive corrective therapy if the patient is a transplant candidate. Patients with well-compensated liver disease and even ESLD may be appropriately treated with TIPS, surgical shunts, or medical therapy first and in the acute setting as a temporizing measure. Despite the shortage of donor organs and morbidity and mortality associated with liver transplantation,

Conclusions

Development of varices due to portal hypertension is a common and often life-threatening occurrence in patients with cirrhosis. Primary prophylaxis is critical in this patient population because of the mortality rate associated with variceal rupture. When prophylactic treatments fail, endoscopic and endovascular interventions allow for reliable, noninvasive means of hemorrhagic control. Surgical decompression provide excellent hemorrhage control and is reserved for recurrent bleeding or for

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