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Nonalcoholic Fatty Liver Disease: What Nurses Need to Know

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Nonalcoholic Fatty Liver Disease: What Nurses Need to Know 1.5 0.5 ANCC CONTACT HOURS PHARMACOLOGY CREDITS Nonalcoholic fatty liver disease: What nurses need to know BY VINCENT M. VACCA, JR., MSN, RN Abstract: Nonalcoholic fatty liver disease AFFECTING UP TO 100 million peo- (NAFLD) is defined as storage of excess ple in the US and up to 35% of the fat in the liver not caused by heavy alcohol population worldwide, nonalcoholic consumption. Nonalcoholic steatohepatitis fatty liver disease (NAFLD) is defined is the severe form of NAFLD. This article discusses causes, diagnosis, and nursing as storage of excess fat in the liver interventions for patients with either not caused by heavy alcohol con- disorder. sumption. Nonalcoholic steatohepa- titis (NASH) is the more severe form Keywords: cirrhosis, diabetes mellitus, of NAFLD. Unlike NAFLD, NASH is fatty liver disease, hepatic fibrosis, insulin characterized by significant hepatic resistance, magnetic resonance elastography, inflammation.2 An estimated 10% to NAFLD, NAFLD Activity Score, NASH, 20% of people with NAFLD develop nonalcoholic fatty liver disease, nonalcoholic NASH (see How fatty liver develops).1,4 steatohepatitis, transient elastography Worldwide, the number of people age 65 or older is projected to in- crease from 524 million in 2010 to nearly 1.5 billion in 2050. Because advanc- ing age is a major risk factor for NAFLD, its incidence is expected to increase as the population ages. NAFLD and NASH are now leading indications for liver transplantation in the US.5-8 This article discusses causes, diagnosis, and nursing interventions for patients with NAFLD and NASH. SHUTTERSTOCK / TEFI 32 l Nursing2020 l Volume 50, Number 3 www.Nursing2020.com Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. www.Nursing2020.com March l Nursing2020 l 33 Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. Metabolic syndrome and • fasting plasma glucose (FPG) damage from alcohol, drugs, and other risk factors 100 mg/dL (5.6 mmol/L) or more, toxins, and less able to regenerate NAFLD is a complex disease dictated or drug treatment for elevated blood or tolerate transplantation.8,11,12 Ad- by both genetic and acquired fac- glucose. ditional stressors affecting the aging tors, including metabolic syndrome Currently, up to 25% of the US liver include systemic metabolic dis- (also called insulin resistance syn- population is affected by metabolic eases and disorders, such as systemic drome). NAFLD is considered the syndrome and approximately 90% inflammation, insulin resistance, hy- hepatic manifestation of metabolic syn- of patients with NAFLD have more pertension, type 2 diabetes mellitus, drome.3,8-10 Under criteria established than one feature of metabolic syn- and obesity.11,12 by the National Cholesterol Education drome.8,11 Metabolic syndrome is as- The loss of hepatocytes associated Program (NCEP) Adult Treatment sociated with cardiovascular disease with the aging process leads to re- Panel III (ATP III), metabolic syndrome and type 2 diabetes. ductions in serum levels of albumin is defined as the presence of any Here is a closer look at major risk and increases in alkaline phospha- three of the following five factors.10 factors associated with NAFLD and tase and aminotransferase levels. • abdominal obesity, defined as a NASH. The metabolism of cholesterol in the waist circumference of 102 cm • Older age. Aging is a significant liver also decreases with the aging (40 in) or more in men and 88 cm risk factor for several chronic liver process, increasing blood cholesterol (35 in) or more in women. diseases and disorders, including levels over time.7 • serum triglycerides 150 mg/dL NAFLD and NASH.7,12 Recent stud- • Obesity. Approximately 30% of (1.7 mmol/L) or more, or drug treat- ies show increased rates of NAFLD obese patients and up to 90% of ment for elevated triglycerides. among older adults compared with morbidly obese patients have a fatty • serum high-density lipoprotein younger patients.12,13 liver.5,6 However, not all patients (HDL) cholesterol less than 40 mg/ Because of age-related cellular, with NAFLD are overweight or dL (1 mmol/L) in men and less than tissue, and functional changes in obese. From 8% to 10% of NAFLD 50 mg/dL (1.3 mmol/L) in women, the aging liver, older patients have patients have a body mass index of or drug treatment for low HDL cho- significantly worse disease than less than 25 and are considered lean, lesterol. younger patients. With advancing supporting the role of genetics in • BP 130/85 mm Hg or more, or age, the liver loses functional capac- development of the disease.4 drug treatment for elevated BP. ity, becoming more susceptible to • Diabetes mellitus. An estimated 1 in 10 middle-aged American adults 11 30 has diabetes mellitus. In a large How fatty liver develops prospective study, patients with dia- Fatty liver is caused betes were shown to have a signifi- by an accumulation of cantly higher incidence of NAFLD triglycerides in liver cells. and hepatocellular carcinoma (HCC) Normally, liver cells contain than individuals without diabetes.11 some fat, which is either Along with cardiovascular disease, oxidized and used for malignancies are common causes of energy or converted to death in patients with NAFLD and triglycerides. This fat is NASH.13 derived from free fatty • acids released from Insulin resistance (IR). Charac- adipose tissue. Abnormal terized by a widespread diminished accumulation occurs cellular response to insulin, IR is when the delivery of free both a key component of metabolic fatty acids to the liver is syndrome and a risk factor for increased, as in starvation NAFLD.5 Normally, insulin is re- and diabetes mellitus, or leased in response to food con- when the intrahepatic metabolism of lipids is disturbed, as in alcoholism. sumption and increased blood glu- The liver shown here was harvested from a patient with risk factors for cose levels, promoting cellular up- nonalcoholic fatty liver disease. It has the characteristic swollen and yellow take of glucose in skeletal muscle, appearance of fatty liver disease. The biopsy showed moderate large-droplet adipose tissue, and the liver. With steatosis but no steatohepatitis or fibrosis. IR, cells cannot readily absorb glu- Photo courtesy of Dr. Amit Mathur, Transplantation Surgery, Mayo Clinic Arizona. cose from the bloodstream, leading 34 l Nursing2020 l Volume 50, Number 3 www.Nursing2020.com Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. to hyperglycemia. Hyperglycemia • Other factors. Additional known stimulates further insulin produc- risks for development of NAFLD tion, resulting in hyperinsulinemia.6 include inflammatory bowel disease, The combined effect of hyperinsu- inborn errors of metabolism, and linemia and IR leads to increased occupational exposure to toxins such free fatty acid in the liver and in- as organic solvents.7 creased production of triglycerides, which can cause or worsen hepatic Notes about NASH steatosis.5,14 Up to 20% of patients with NAFLD The presence of IR is an inde- progress to NASH, which is associ- pendent predictor of advanced liver ated with hepatic tissue damage, in- fibrosis in patients with NAFLD.7 flammation, cirrhosis, hepatocellular Due to the strong association be- necrosis, and liver failure.4,7,18 tween reduced insulin sensitivity and Cirrhosis is a late stage of hepatic increased incidence of cardiovascu- fibrosis and is generally consid- lar disease with NAFLD, diabetes ered to be irreversible in advanced screening for patients with NAFLD stages.19 NASH is associated with is suggested.8 rapid progression of liver fibrosis and • Obstructive sleep apnea (OSA). the potential to develop HCC and Hypoxia secondary to OSA has been eventual liver failure.4,5,7,11 Cirrhosis linked to IR and lipogenesis, causing is present in 70% to 90% of patients a systemic proinflammatory state. with HCC. According to the World Recent research has linked the pres- The most common initial Health Organization, HCC is the fifth ence and severity of hypoxia second- signs and symptoms of most common cancer worldwide and ary to OSA to the severity of liver NAFLD are nonspecific, was the second most common cause 14 11 fibrosis associated with NASH. such as fatigue, and do of cancer-related death in 2015. • Polycystic ovary syndrome (POS). Morbidity from NASH is on the This disorder is also associated with not correlate to disease rise. Cirrhosis caused by NASH in- IR. Because 55% of women with POS severity. creased 170% for individuals on the present with NAFLD, women with US liver transplant waitlist between POS should be evaluated for NAFLD.8 urated fats, high-fat dairy products, 2004 and 2013. NASH-associated • Gender. The incidence of NAFLD and sugary beverages are associated cirrhosis is now the second leading is known to be higher in males and with a greater likelihood for develop- indication for liver transplantation in postmenopausal females than other ment of metabolic disorders such as the US.15 groups.7 type 2 diabetes, obesity, and IR—all • Drugs. NAFLD can be triggered by of which can progress to NAFLD and Assessment and diagnosis many medications, such as amioda- NASH.7,14 The most common initial signs and rone, aspirin, estrogens, glucocorti- In addition, excessive calorie in- symptoms of NAFLD are nonspe- coids, methotrexate, tamoxifen, and take can result in accumulation of cific, such as fatigue and malaise, tetracycline.7 excessive triglycerides and free fatty and do not correlate to the severity • Genetic factors. Recent evidence acids in the liver, leading to hepatic of disease. Some patients report pain supports a strong genetic connection steatosis.7 This effect is known in the right upper abdomen early in between development of NAFLD and to occur rapidly, within days to disease. Hepatosplenomegaly is pres- progression to NASH.13,15,16 Ethnic- weeks.6,7 One study of patients re- ent in up to 50% of patients; how- ity is also considered to be a risk fac- ferred to an urban hospital-based ever, as the disease progresses, the tor, with Hispanic individuals being lipid clinic showed a NAFLD preva- liver shrinks in size and the spleen more susceptible than people in non- lence of 50%.5 Excessive calorie enlarges.
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