Physiology and function

In general, the liver is the biochemical engine of metabolism. The liver receives one-third of the total cardiac output. The hepatic artery carries 25 percent, the portal vein 75 percent, with the liver subsequently receiving 1.5 L of blood per minute.5 All blood traverses the liver via the portal triads and travels via the hepatic sinusoids to ultimately arrive in the hepatic veins and vena cava. Under normal circumstances, pressure in the portal vein is low, 9-12 mmHg; however, a pressure gradient still exists toward the vena cava, where the central venous pressure generally reaches zero. To allow for the large volume of blood to disperse through the liver, the vascular resistance in the hepatic sinusoids is low. In diseased states, the resistance conversely can increase resulting in high-portal pressure and shunting of blood around the liver via collaterals. Portal hypertension results from any condition that increases prehepatic venous pressures greater than 12 mmHg.

Extended right lobectomy Right lobectomy Right trisegmentectomy

Right lobectomy Right hepatectomy

Right lobectomy Right hepatectomy

Left lobectomy Left hepatectomy

Extended left lobectomy Extended left hepatectomy Left trisegmentectomy

Figure 11-4 Resection planes for hepatic resections with alternative nomenclatures. (Source: Used with permission from Vauthey JN. Liver imaging: a surgeon's perspective. Rad Clin North Am 36:445-457, 1998.)

Portal hypertension can be divided into three main causes: presinusoidal, intrasinusoidal, or postsinusoidal. The most common causes of each respectively are portal vein thrombosis, cirrhosis, and hepatic vein occlusion (Budd-Chiari syndrome). Complications of portal hypertension the include esophageal and gastric varices, encephalopathy, and ascites. Ascites (or accumulation of intraabdominal fluid) is thought to be secondary to the effects of portal hypertension on increasing splanchnic blood volume as well as the increased secretion of aldosterone.6

Nutrients such as proteins, sugars, and fats are metabolized by the liver, but toxins such as various ingested poisons (alcohol, medications, and so on) and gut bacteria translocating through the bowel wall are cleared by the liver as well. Ultimately, the hepatocyte is the core unit of the metabolic machinery. The filtering proportions of sinusoidal endothelial cell, and specialized liver macrophages, Kupffer cells, aid the hepatocyte. The specific role of the hepatocyte is determined by the position of the cell in the hepatic architecture relative to the distance from the portal triad or the hepatic venule. It has become clear that hepatocytes in one area of the liver can be recruited to fulfill tasks in an adjacent area, essentially providing for a continuum, with each hepatocyte capable of providing the full spectrum of necessary functions based on demand.

Detoxification is one of the major functions of the liver, and important enzyme systems exist to break down substances that are toxic to the body. One of the main systems is the cytochrome p450 system, which aides in oxidative break down of toxic metabolites. Certain medications can induce the cytochrome p450 system, as they are toxic, or inhibit the enzyme system and thereby influence the metabolism of other drugs. This can be very important clinically as patients with histories of substance abuse (i.e., alcohol) will have an induced cytochrome p450 system, which increases the metabolism of pain medications, and some anesthetics affecting their clinical management.

Carbohydrate metabolism is one of the core functions of the liver. As energy supply is not constant, the body has to adapt to irregular food intake by devising a system whereby energy can be stored and called upon on demand. The liver provides this function by storing glucose in the form of glycogen in hepatocytes. In situations where the body needs more energy than is currently being ingested or during times of fasting, glycogen is used for neogenesis of glucose. Even in unfavorable situations such as anaerobic metabolism, the liver will continue to provide energy by recycling lactic acid, a product of anaerobic metabolism, into glucose via the Cori cycle.7 The liver is also a key structure in fat and protein metabolism. Maintaining close communications with adipocytes via cell signaling pathways, the liver regulates fat storage and reabsorption as a more long-term storage of energy. By producing and breaking down amino acids, the liver is primarily responsible for maintaining nitrogen balance in the body. The liver produces more than 5000 proteins, varying from albumin to clotting factors. The importance of the liver as a protein factory becomes relevant in diseased states, when severe hypoalbuminemia and increased clotting times complicate clinical care of the patient with liver disease.

As discussed earlier, the liver produces bile, both as a route to eliminate waste as well as to aid in digestion. One of the main components is bilirubin, derived from the breakdown of hemoglobin. In the systemic circulation bilirubin is bound to albumin, taken up by the liver and conjugated with glucuronic acid in the hepatocyte. Next, the bilirubin is secreted into bile and transported away from the hepatocytes, ultimately to the duodenum. For the most part bilirubin is eventually reabsorbed downstream in the intestinal tract after it has been deconjugated and converted into urobilinogen. Only 5 percent of the bilirubin, converted to urobilinogen by gut bacteria, is excreted with feces, giving it its characteristic brown color. Some of the reabsorbed urobilinogen is excreted with urine, coloring it yellow. Based on where the bilirubin pathway is interrupted, due to liver disease, stones, or reabsorption, either conjugated, or unconjugated bilirubin concentrations will rise in serum and cause jaundice. At concentrations of 2.5 mg/dL initially the scle-rae become yellow, but at higher concentrations the skin and entire body will become discolored. An important caveat when examining patients with liver disease is that fluorescent lighting can lead to an erroneous diagnosis of scleral icterus; examinations of patients in natural lighting will remove this potential for error.

Normally, there is uninterrupted flow of bile from the liver to the gallbladder and subsequently, the duodenum. There is an intricate interaction between the gallbladder and duodenum, via nervous and hormonal pathways. Based on the amount and consistency of food delivered into the duodenum by the stomach, a certain amount of bile will be excreted from the gallbladder. The migrating myoelectric complex (MMC) is a nervous electrical wave essentially propulsing food downstream, mediated by hormonal signals (Motilin). It also induces gallbladder contraction. Another mechanism to release bile into the duodenum is cholecystokinin (CCK), a hormone that directly induces gallbladder contraction and is released by the duodenum. By virtue of the sphincter of Oddi, the sphincter at the end of the common bile duct, as it enters the duodenum, a fairly constant pressure of 15 mmHg is maintained in the bile ducts. Opening and closing of the sphincter of Oddi is also closely regulated by CCK and Motilin.8

Bile consists of three major components: bile salts, cholesterol, and water. An equilibrium among these components exists, allowing for the maintenance of flow and the proper digestive properties of bile. Any imbalance in the three components can lead to insolubility resulting in stones and their related disease states.

Of the thousands of proteins the liver produces, the proteins that comprise the coagulation system are of utmost importance. Various proteins are involved in a cascade-like fashion to produce a rapid response to injury. A

detailed description of the proteins produced by the liver is beyond the scope of this text; however, a common finding in patients with severe disorders of the liver is an elevated prothrombin time (PT).

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