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CHAPTER 18 The liver and gallbladder in the geriatric population
Gary Trey
Gastroenterology and Hepatology, Beth Israel Deaconess Hospital, Boston, Massachusetts, USA; Cambridge Health Alliance, Cambridge, Massachusetts, USA; Harvard medical School, Boston, Massachusetts, USA
Introduction
The liver, unlike any other organ, can regenerate itself after injury. This is essential to its function as, via the portal circulation, the liver is exposed to toxins that are eaten and produced by bacteria in the gut. The liver as such is less affected by age than other organs. A recent article noted that using livers from donors older than 70 should not be discouraged because of good survival rates.1 Age‐related pathophysiologic changes in the liver include hepatic hypoperfusion, decreased liver size, reduced activity of phase 1 drug‐metabolizing enzymes, compromised hepatic regeneration, relative dilation of the common bile duct, and increased lithogenicity of bile.2,3
Many liver diseases take decades to go from asymptomatic to symptomatic. Hepatobiliary diseases are prevalent in the elderly. The rate of mortality from chronic liver disease was highest among patients age 65–74 (49 per 100,000 men, 26.7 per 100,000 women). These rates are 3.2‐ and 5.6‐fold higher than those for men and women age 35–44.4 Liver and gallbladder diseases that occur in the elderly are not substantially different from those in younger populations. Although there are no liver diseases specific to advanced age, the presentation, clinical course, and management of liver disease in the elderly may differ in important respects from those of younger individuals.
Liver diseases prevalent in the elderly include alcoholic liver disease (ASH), nonalcoholic hepatic steatosis (NASH), chronic hepatitis B and C, and others. Particular attention has to be given to drug‐induced liver injury (DILI), which increases in prevalence with age due to increased polypharmacy and the ageing liver's decreased ability to detoxify medications. So, the likelihood of patients having decompensated liver disease increases with age. Therefore, our discussion of liver and gallbladder disease needs to cover the natural history of the most common liver and gallbladder ailments with special emphasis on diet‐, drug‐, and alcohol‐induced liver disease.
Perhaps the best way to understand liver diseases is to start with the clinical presentations of liver disease to a gerontology practice and then go over their workup, differential diagnosis and treatment. Liver disease usually present in several manners: asymptomatic increased liver enzymes or clinical symptomatology such as jaundice, ascites, gastrointestinal haemorrhage, encephalopathy, abdominal pain, or sepsis. We look at each of these presentations: the differential diagnosis, specific diseases and treatments.
The most common presenting complaint to a hepatology practice is abnormal transaminases in asymptomatic patients. Alcoholic liver disease, advanced cirrhosis, and muscle breakdown from exercise are reasons to present with aspartate aminotransferase (AST) greater than alanine aminotransferase (ALT). Most other liver diseases present with ALT greater than AST. Most patients present with abnormal transaminases and relatively normal bilirubin and alkaline phosphatase. This pattern is seen when there has been damage to the hepatocytes and not to the canalicular or bile duct cells. The most common reason to see this abnormality is fatty liver disease. Elevations in alkaline phosphatase primarily occur in cholestasis, which can be due to blockage of the biliary system by stones or tumours, immunologic diseases of the biliary system (primary biliary cholangitis and primary sclerosing cholangitis), or space‐occupying masses.
Acute hepatitis is a sudden syndrome of jaundice, fatigue, and elevated liver enzymes that can be caused by drug reactions, viruses, alcohol, or autoimmunity. The severity of the syndrome can be judged by the level of increase of the prothrombin time (after repletion of vitamin K), as this clotting factor is dependent on substances produced in the liver and to a lesser extent by the levels of bilirubin, transaminases, and albumin.
Cirrhosis is the condition in which considerable liver tissue is replaced by connective tissue, resulting in fibrosis, stiffness of the liver, and portal hypertension. The portal vein supplies the liver with 70% of the blood supply, and the hepatic artery 30%. When the liver is cirrhotic, the pressure in the portal vein increases from normal of about 4 to 10 or higher. When this pressure is greater than 10, a person can have decompensated cirrhosis: ascites, encephalopathy, or variceal bleeding. It is also important to realize that cirrhosis is a premalignant condition, with about 30% of cirrhotics getting liver cancer. Cirrhosis in most people has a long asymptomatic stage before decompensation, referred to as compensated cirrhosis. These patients need to be identified, as they are at risk for decompensation with encephalopathy, hepatocellular carcinoma, and variceal bleeding. We have methods of preventing variceal bleeding, treating encephalopathy, and detecting liver cancer early, at a curable stage.
Fibrosis severity should be determined in all patients with chronic liver disease, as it predicts clinical outcomes and designates patients with cirrhosis who are usually asymptomatic but are at risk for sudden complications or bleeding varices, encephalopathy, and liver cancer. While biopsy is the gold standard method to stage fibrosis, noninvasive methods have been developed that can assess disease severity. In grading a biopsy for fibrosis, the most common criteria are from the METAVIR system:no fibrosis is F0, and cirrhosis is F4. Hepatic decompensation does not usually occur until the patient has cirrhosis. Liver biopsies are painful and have a mild risk, so non‐invasive ways have been developed to estimate the METAVIR score. The FIB‐4 index uses a combination of four factors to estimate fibrosis: age, platelet count, and levels of AST and ALT, according to this formula:
Applications can be easily found on smartphones and online to perform the calculations.5 The AST‐to‐platelet ratio index (APRI) score with a cutoff value of less than or equal to 0.5 had a negative predictive value of 86% for the absence of significant fibrosis, while a
