Hepatic cirrhosis results from fibrous scarring mixed with hepatocellular regeneration in response to sustained inflammatory, toxic, metabolic, and congestive insults. Over time, the functional anatomy of the liver is replaced by scar tissue isolating nodules formed by foci of regenerating hepatocytes. Normal function of the liver is dependent not only on preservation of hepatocyte number but also on the elaborate microscopic architecture of the functional hepatic units. In addition to progressive loss of synthetic and metabolic function, scarring and degeneration of the liver contribute to increased resistance to blood flow from the splanchnic circulation, contributing to portal-systemic shunting and portal hypertension. Shunting isolates the remaining functional tissue of the liver, further contributing to the metabolic derangements that characterize progressive and end-stage liver disease. Emergent complications of cirrhosis and end-stage liver disease include gastroesophageal variceal hemorrhage, refractory ascites and spontaneous bacterial peritonitis, hepatorenal syndrome, and hepatic encephalopathy. -I9
Gastroesophageal Varices and Hemorrhage Cirrhosis results in a progressive increase in resistance to portal blood flow through the liver and shunting of blood through venous collaterals into the systemic circulation. Increased blood flow and pressure in these collateral veins contribute to the formation of submucosal varices in the gastric fundus and esophagus. These superficial and thin-walled varices are prone to ulceration and hemorrhage. Gastroesophageal variceal hemorrhage is a common and dangerous complication of hepatic cirrhosis and portal hypertension. The prevalence among cirrhotics is approximately 25 to 70 percent. Acute hemorrhage carries a 30 to 60 percent mortality rate.
Hemorrhage is heralded by hematemesis, hematochezia, and/or melena, plus varying degrees of hemodynamic instability. Complicating factors include preexisting anemia, thrombocytopenia, and coagulopathy. The differential diagnosis of acute gastrointestinal hemorrhage in the cirrhotic is less important than identification of a condition that requires aggressive managment and appropriate consultation. Basic priorities in management include airway protection and appropriate intravenous access for the infusion of fluids and blood products. Significant coagulopathy should be assumed, and placement of central venous catheters should be performed with extreme caution. Gastric lavage is indicated when active bleeding is suspected to evacuate the stomach and help alleviate repeated vomiting, which can exacerbate hemorrhage. Gastric lavage provides some indication of the location of hemorrhage and a gross assessment of ongoing blood loss. The presence of known gastroesophageal varices is not a contraindication to the careful placement of a nasogastric or orogastric tube. Consultation for emergent endoscopy should be arranged as soon as possible. Endoscopy provides a definitive diagnosis and often a direct means for hemorrhage control by sclerotherapy. Unavailability of such consultation should prompt consideration of early transfer.20
In addition to the replacement of blood loss with fluids and blood products, the pharmacologic agents vasopressin and somatostatin have been shown to be useful short-term measures to stem variceal hemorrhage (see T§bJ.e,..82.:6). Both agents produce a reduction in portal venous blood pressure, although by importantly different mechanisms. Vasopressin causes splanchnic arteriolar constriction, reducing portal venous inflow and pressure. Somatostatin decreases splanchnic blood flow by causing a direct and selective relaxation of mesenteric vascular smooth muscle. Vasopressin action is nonspecific and has potential for undesireable cardiac and hemodynamic side effects, particularly in older individuals. Coronary vasospasm can cause cardiac ischemia, infarction, and arrhythmias. There is also potential for stroke and mesenteric and limb ischemia. To attenuate these complications, some authorities recommend the coadministration of nitroglycerin by continuous intravenous infusion starting at 40 pg/min and titrating upward for a systolic blood pressure of more than 100 mmHg. Terlipressin is a synthetic derivative of vasopressin that is slowly converted to vasopressin in vivo. Terlipressin has a much longer half-life than vassopressin and has been shown to be superior in a comparison study. This drug is not widely available, but the studied treatment protocol used 1 to 2 mg IV every 4 to 6 h and was compatible with the coadministration of intravenous nitroglycerin.20,21 and 22
Somatostatin has been demonstrated to be effective in reducing variceal bleeding without significant adverse side effects. The short half-life of somatostatin (1-2 min) has limited its usefulness. Octreotide (Sandostatin), an analogue of somatostatin, has been demonstrated to be as effective as injection sclerotherapy in the management of acute variceal hemorrhage and is considered by many to be a useful primary therapy and adjunct to sclerotherapy. Octreotide may be particularly beneficial in the management of hemodynamically unstable patients undergoing resuscitation but unable to tolerate emergent endoscopy. Octreotide has minimal hemodynamic side effects, giving it a distinct advantage over vasopressin 2 2 and 23 (T§bJ®..82.-6).
Balloon tamponade with inflated gastroesophageal obturators such as the Sengstaken-Blakemore tube is used infrequently because of the high rate of complications and the increasing effectiveness and availability of endoscopic sclerotherapy. Principal complications of these devices include bronchopulmonary aspiration and esophageal rupture. b Blockers and portosystemic shunt surgery or transjugular intrahepatic portosystemic shunts (TIPS) are effective prophylactic measures in some patients with gastroesophageal varices but have no proven role in the management of acute gastroesophageal hemorrhage.
Ascites and Spontaneous Bacterial Peritonitis Ascites and anasarca occur in hepatic cirrhosis as a result of portal hypertension, impaired renal sodium and water excretion, and hypoalbuminemia. When extreme, ascites may cause immobility, abdominal pain, and respiratory compromise. Umbilical hernia is common in this setting, and hernia ulceration with rupture, although rare, is a life-threatening complication. 24 Primary or spontaneous bacterial peritonitis (SBP) is the most frequently encountered complication of cirrhotic ascites, with a yearly risk of approximately 29 percent. The presentation of SBP usually includes fever, abdominal pain, and diffuse abdominal tenderness, but it may be relatively silent and present only with subacute functional decline or worsening in baseline encephalopathy 2627 (Table
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