ss abe, CURRICULUM ON ALCOHOLIC LIVER DISEASES FOR NURSES “—¢INDEX S.No Contents Page no. 1 Chapter-I: Introduction to Alcoholic 2 Liver Diseases p Chapter-2: Alcoholic Fatty Liver m (Steatosis) 3 Chapter-3: Alcoholic Hepatitis R 4 Chapter-4: Alcoholic Cirrhosis 15 , Chapter-5: Complications and nurses’ 19 role in Alcoholic Liver Diseases 4 Chapter-6: Liver Transplantation 26CHAPTER-1 Introduction to Alcoholic Liver Diseases The relationship of alcohol consumption and liver diseases is well established. It can cause hepatocellular damage through toxic ethanol metabolism-associated mechanisms and malnutrition. Alcohol is one of the most frequent causes of liver disease; alcohol-involved subtypes of liver disease include alcoholic hepatitis, steatosis, steatohepatitis, fibrosis and cirrhosis. Acute alcoholic hepatitis and liver cirrhosis are associated with high mortality (which can reach $0% in acute alcohol hepatitis), and the median survival time of patients with advanced liver cirrhosis can be as low as 1-2 years The aleoholic liver disease covers a spectrum of disorders beginning from the fatty liver, progressing at times to alcoholic hepatitis and culminating in alcoholic cirthosis, which is the most advanced and irreversible form of liver injury related to the consumption of alcohol. ‘As per the histologic stages of alcoholic liver disease it is divided in to three 1. Alcoholic Fatty Liver or Steatosis- At this stage, fat accumulates in the liver parenchyma, 2, Alcoholic Hepatitis - Inflammation of liver cells take place at this stage, and the ‘outcome depends on the severity of the damage. Alcohol abstinence, nutritional support, treatment of infection, and prednisolone therapy in severe cases can help in the treatment of alcoholic hepatitis, but more severe cases lead to liver failure. 3. Alcoholic Cirrhosis - Liver damage at this stage is irreversible and leads to complications of cirrhosis and portal hypertension”! Alcohol absorption and metabolism. Alcohol (ethanol) is readily absorbed from the stomach, but most is absorbed from the small intestine. Alcohol cannot be stored. A small amount is degraded in transit through the gastric mucosa, but most is catabolized in the liver, primarily by alcohol dehydrogenase (ADI) but also by cytochrome P-450 2E1 (CYP2E1) and the microsomal enzyme oxidation system (MEOS). Metabolism via the ADH pathway involves the following: + ADH, a cytoplasmic enzyme, oxidizes alcohol into acetaldehyde. Genetic polymorphisms in ADH account for some individual differences in blood alcohol levels after the same alcohol intake but not in susceptibility to alcoholic liver disease. + Acetaldehyde dehydrogenase (ALDH), a mitochondrial enzyme, then oxidizes acetaldehyde into acetate. Chronic alcohol consumption enhances acetate formation. Asians, who have lower levels of ALDH, are more susceptible to toxic acetaldehydeeffets (¢.g., flushing); the effects are similar to those of disulfiram, which inhibits ALDH. + These oxidative reactions generate hydrogen, which converts nicotinamidk dinucleotide (NAD) to its reduced form (NADH), increasing the redox potential (NADH/NAD) in the liver. + The iner -d redox potential inhibits fatty acid oxidation and gluconcogen promoting fat accumulation in the liver. Chronic alcoholism induces the MEOS (mainly in endoplasmic reticulum), increasing its activity. The main enzyme involved is CYP2E1. When induced, the MEOS pathway can account for 20% of alcohol metabolism, This pathway generates harmful reactive oxygen species, increasing oxidative stress and formation of oxygen-free radicals." Etiology Metabolic, genetic, gender,environmental, and immunological factors play a major role in alcoholic liver disease The liver tolerates mild aleohol consumption, but as the consumption of alcohol inereases, it leads to the disorders of the metabolic functioning of the liver. The initial stage involves the accumulation of fat in the liver cells, commonly known as fatty liver or steatosis. If the consumption of alcohol does not stop at this stage, it sometimes leads to alcoholic, hepatitis. With continued alcohol consumption, the alcoholic liver disease progresses to severe damage to liver cells known as "alcoholic cirrhosis." Alcoholic cirrhosis is the stage described by progressive hepatic fibrosis and nodules. Quantity and duration of the patient's alcohol intake are the highest risk factors for the development of the liver disease. The beverage type plays a minimal role. Women are more susceptible than men, Obesity and high-fat diet also increase the risk of alcoholic liver disease. Concurrent hepatitis C infection is associated with younger age of onset, more advanced histological damage, and decreased survival. Patatin-like phospholipase domain- containing protein 3 (PNPLAP3) is associated with alcoholic liver cirrhosis.! Pathophysiology Alcohol metabolism by the liver is primarily via two enzymes: 1. Alcohol dehydrogenase 2. Aldehyde dehydrogenase Alcohol dehydrogenase converts alcohol into the acetaldehyde, and aldehyde dehydrogenase converts acetaldehyde into the acetate, The metabolism of alcohol increases the production of NADH by reducing NAD in the body. This shifting of metabolic balance toward the production of NADH leads to the formation of glycerol phosphate, which combines with the fatty acids and becomes triglycerides, which accumulate within the liver. When lipidoxidation (lipolysis) stops due to alcohol consumption, fats accumulate in the liver and lead to "fatty liver disease." Continued alcohol consumption brings the immune system into play. Interleukins with the help of neutrophils attack the hepatocytes, and swelling of the hepatocytes known as the “alcoholic hepatitis" takes place. Ongoing liver injury leads to irreversible liver damage, the citthosis of the liver.”! Assessment of Alcoholic Liver Diseases It includes detail history collection, Physical examination and laboratory investigation. History Collection Drinking history is an essential component, which includes the number of drinks per day and the duration of drinking. Given the lack of a unique diagnostic test, the exclusion of other causes of liver injury is mandatory. Personal and psychosocial factors are also important because excessive drinking is related to depression and other psychological diseases. Patients should be asked about diet, alcoho! consumption, caloric intake, risk factors for malnutrition, and risk factors for chronic liver diseases such as viral hepatitis. ‘+ Nurses should explore signs and symptoms, including: ‘+ Nausea and vomiting * Abdominal pain or discomfort ‘+ Loss of appetite ‘+ Weight loss or weight gain + Thereased thirst ‘+ Yellowish discoloration of eyes + Weakness ‘Fever (in alcoholic hepatitis) * Confusion ‘+ Alteration of the sleep-wake cycle ‘+ Mood swings * Fainting Physical Examination The clinical definition of alcoholic hepatitis is a syndrome of liver failure where jaundice is a characteristic feature; fever and tender hepatomegaly are often present. The typical presentation age is between 40 and 50 years, and it occurs in the setting of heavy alcohol use. Patients often report a history of intake of at least 30 to 50 g alcohol/day though over 100 g/day is common. Patients may be abstinent for weeks before admission. The cardinal sign is the rapid onset of jaundice. Other signs and symptoms include fever, ascites (SAAG greaterthan 1.1), and proximal muscle loss. Patients presenting with severe alcoholic hepatitis may have encephalopathy. Typically, the liver is enlarged and tender. General physical examination typically shows jaundice, hepatomegaly, splenomegaly, spider telangiectasias, Dupuytren contractures, testicular atrophy, decreased libido, parotid and lacrimal gland enlargement, white nails, Muecke lines, asterixis and features of portal hypertension such as ascites, pedal edema, encephalopathy and caput-medusae (distended and. engorged superficial abdominal veins) Abdominal paracentesis should be performed in all patients with newly identified ascites. Laboratory Investigation "BC (Complete blood count) to rule out the infection, look for complications of cirhosis: anemia, thrombocytopenia, a leukemoid reaction in alcoholic hepatitis. + LFTs (liver function tests): AST (aspartate aminotransferase) is markedly raised as opposed to ALT (alanine aminotransferase) in alcoholic liver disease. There is hypoalbuminemia, hyperbilirubinemia, and hypertriglyceridemia, Also, GGTP (gamma-glutamyltranspeptidase) is usually raised. + Prothrombin time (PT) and INR (to assess liver synthetic function): an elevated value indicates more severe disease. + Abdominal imaging (abdominal ultrasonography) is useful in looking for biliary obstruction and liver tumors. + BMP (basic metabolic profile) should be ordered to look for renal failure and electrolyte disturbance (low levels of potassium, magnesium, and phosphorus). + Ascitic fluid SAAG (serum-ascites albumin gradient) should be calculated to assess the reason for ascites if present. ‘+ Screening blood tests for other causes of chronic liver disease, including viral hepatitis + Endoscopy to look for esophageal varices due to portal hypertension in patients with cirthosis. + A liver biopsy can lead to a definitive diagnosis in cases where the diagnosis is Uncertain, More often than not, itis used for evaluation of severity, prognosis, staging, and treatment monitoring. For an accurate diagnosis of ong sample of liver tissue is necessary. Liver biopsy has a risk of complication, including life-threatening hemorthage, so it is reserved for cases where results of a biopsy can make a difference in the treatment plan. rosis, at least 1.5 to 2.em Symptoms and signs in alcoholic Liver Disease There are different signs and symptoms in ALD. These are as follows‘Symptoms ‘© Upper abdominal pain, particularly right upper quadrant ‘© Nausea with or without vomiting © Anorexia © Malaise © Fatigue = Dark urine = Fever '* Confusion, disorientation ‘Signs ‘* Hepatomegaly, often tender = Jaundice = Fever © Tachycardia + Tachypnea © Ascites * Edema © Caput medusae ‘© Parotid and lacrimal gland enlargement © Asterixis © Spider nevi + Gynecomastia Laboratory abnormalities in alcoholic liver disease Typical laboratory findings in ALD include transaminase levels with aspartate aminotransferase greater than alanine aminotransferase as well as increased mean corpuscular volume, gamma-glutamyltranspeptidase, and IZA to IgG ratio, In unclear c: s, the diagnosis can be supported by imaging and liver biopsy. The histological features of ALD can ultimately define the diagnosis according to the typical presence and distribution of hepatic steatosis, inflammation, and Mallory-Denk bodies.) Serum enzymes Serum proteins AST 2ALT with ratio | Serum albumin is normal os until liver injury is significant AST <400 1U and Carbohydrate-deficient transferrin is elevated ALT <200 10 depending on recentconsumption Alkaline phosphatase elevated toa variable | Cytokeratin 18 is elevated degree including M30 and M65 fractions v-glutamyl transferase | Serum immunoglobulin A elevated toa variable | (IgA) is elevated degree depending on | _ Serum immunoglobulin G recent consumption _| (IgG) is modestly elevated Hematologic abnormalities Mild anemia Elevation in mean corpuscular volume (mev) Platelets may be decreased due to alcohol ‘marrow toxicity or portal hypertension White blood cell count is elevated in alcoholic hepatitis in absence of overt infection Metabolic and electrolyte ‘abnormalities Hypertiglyceridemia Hyperuricemia Hypokalemia Hypomagnesemia Hypophosphatemia Low serum zincManagement Abstinence and lifestyle modification Treatment of addiction to alcohol is the paramount step in managing ALD. Abstinence from alcohol leads to res lution of alcoholic fatty liver disease (benign steatosis) and abstinence improves survival in alcoholic cirrhotic patients, even those with decompensated liver function. Furthermore, reducing alcohol consumption, but not completely stopping, has been shown to improve survival in patients with ALD. Pharmacotherapy in combination with psychosocial interventions can aid patients in maintaining abstinence from alcohol. ‘Naltrexone and acamprosate have been shown to assist in reducing or eliminating alcohol intake in chronic heavy drinkers along with Brief intervention and active participation in Alcoholics Anonymous Group. Nutritional Support Nutritional support in alcoholic liver disease. ‘Nutritional support for patients with ALD depends on the severity of liver disease, concomitant factors leading to malnutrition (e.g., anorexia and pancreatic insufficiency), and the presence of obesity. Obese patients with less severe liver injury should be referred to a dietician and advised concerning dietary restriction and regular exercise. In outpatient therapy for patients with ALD, nutritional support in alcoholic cirrhotic patients improves nutritional status and cell mediated immunity, as well as decreases infectious complications and consequent hospitalizations. Use of probiotics is unproven, but may be beneficial if patients arcon broad spectrum antibiotics!*! Key points in maintaining nutrition 1. Encourage voluntary oral intake when possible Enteral support with dietary supplements is strongly preferred overparenteral support Feeding tubes should be used only when absolutely necessary Evidence is lacking to support use of parenteral nutrition Protein 1.5 g/kg body weight Total calories of 30 kcal/kg body weight (minimum) © 50-55% as complex carbohydrates + 25-30% as fat, preferably avoiding polyunsaturated fat + 20% as protein 2. Provide night time snack of 500-700 kcal to avoid hepatic 8. glycogen depletion 9. Bcomplex multiple vitamins daily 10. Thiamine 100mg daily 11, Zinc 220 mg/kg unless patients have renal insufficiency 12. Correct magnesium deficiency 13. Correct hypokalemia 14. Correct hyponatremia cautiously.”Medications Glucocorticosteroids represent the most widely accepted therapy in patients with severe ASH (defined as Maddrey’s DF > 32 or MELD score > 21). Corticosteroids plus aggressive enteral nuttition is a reasonable approach to the treatment of patients.!*! Pentoxifylline. This drug reduces blood viscosity and improves microcirculation, In ALD, it also exerts antioxidant effects and inhibits production of tumor necrosis factor. In several clinical trials, pentoxifylline increased 6-month survival and reduced the incidence of hepatorenal syndrome (renal dysfunction related to decreased perfusion with hepatic disease Role of nurse in alcoholic liver diseases + Early identification of liver disease + Provision of support and information for those newly diagnosed (including education on what liver disease means) + Assessment and monitoring of compliance with medication, enabling service users to complete treatments + Advice on lifestyle, health promotion and wellbeing + Support for service users to attend clinics and engage with treatments, such as regular endoscopy and ultrasounds to screen for hepatocellular carcinoma + Support and advice on medication compliance for service users who continue to drink + Links across primary and secondary care to help service user access services such as day case paracentesis + Delivering and monitoring viral eradication therapy in clinics co-located with alcohol and drug services + Provide pharmacological management, which may include dispensing, advii in relation to the service user's prescription for their drug and alcohol problem ind support + Provide expert clinical advice for commissioners, service users, families and care givers, health and other professionals + Provide a clinical perspective to reducing harm from alcohol and drug misuse, promoting and enabling recovery and wellbeing + Mobilize and co-ordinate resources in managing alcohol crises, for example, intoxication, overdose, acute withdrawal states + Provide early identification and interventions for alcohol-related physical illnesses such as alcohol related liver disease (ARLD), alcohol related brain injury (ARBI) and alcohol-relateddementia Provide blood borne virus screening (hepatitis C and HIV) and hepatitis B vaccination + Provide clinical assessments which may include interpretation of test results for example, electro cardiograms (ECG), urinalysis results, blood results References 1, WHO, Global status report on alcohol and health 2018 [Intemet]. [cited 2021 Feb 2);Available from: hutps://www.who intwestempacific/health-topics/alcohol 2. Patel R, Mueller M. Alcoholic Liver Disease [Internet]. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2020 [cited 2021 Feb 2]. Available from: hitp:{/www.nebi.nim.nih.gov/books/NBK546632/ 3. Alcoholic Liver Disease - Hepatic and Biliary Disorders [Intemet]. MSD Man. Prof. Ed, [cited 2021 Feb 2];Available from: https://www:msdmanuals.com/professional/hepatic- and-biliary-disorders/alcoholic-liver-disease/alcoholic-liver-disease 4. Seitz HK, Bataller R, Cortez-Pinto H, Gao B, Gual A, Lackner C, et al. Alcoholic liver disease, Nat Rev Dis Primer 2018;4(1):16. 5. Torruellas C, French SW, Medici V. Diagnosis of alcoholic liver disease. World J Gastroenterol.2014; 6. Frazier TH, Stocker AM, Kershner NA, Marsano LS, McClain CJ. Treatment of alcoholic liver disease. Ther Adv Gastroenterol [Internet] 2011 [cited 2021 Jan 31];4(1)-63-81. Available from: https://www ncbi.tilm.nih, gov/pme/articles/PMC3036962/ 7. Eugene R. Schiff Willis C, Maddrey K. Rajender Reddy. Schiffs Diseases Of Liver, 12th Edition, John Wiley & Sons Ltd; 8. Morrison, Dolores, Sgrillo, Justine, Daniels, Lauren, Managing alcoholic liver disease [Internet]. [cited 2021 Feb 2];Available from: https://nursingeenter.comvinteriormaster/ce-pages/cearticle/ce_articleprint 9. Alcoholic_liver_disease.pdf [Internet]. [cited 2021 Feb 2);Available from: hitps://www-hopkinsmedicine.org/gastroenterology_hepatology/_pdis/livet/alcoholic_liv er_discase.pdf 10, Alcoholic Fatty Liver - an overview | ScienceDirect Topics [Intemet]. [cited 2021 Feb 1);Available from: https://www.sciencedirect.com/topics/medicine-and- dentistry/alcoholic-fatty-liver 11. Catherine Frakes Vozz0, DO, Nicole Welch, MD, Carlos Romero-Marrero, MD, Kyrsten D. Fairbanks, MD. Alcoholic Liver Disease [Internet]. [cited 2021 Jan 31];Availablefrom: hitps://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/ale oholie-liver-disease! 10CHAPTER 2 Alcoholic Fatty Liver (Steatosis) Alcoholic fatty liver is potentially reversible condition in which macrovesicular fat accumulates as large droplets of triglyceride and displaces the hepatocyte nucleus, most markedly in perivenular hepatocytes resulting in the liver enlargement. Alcoholic fatty liver (steatosis) occurs almost universally in individuals who consume alcohol excessively (in the range of 120-150 giday for 2-3 weeks). In most cases macrovesicular steatosis develops; this is initially located in Zone 3 and in severe cases is located throughout the liver. Abstinence for 4 weeks leads to resolution. Usually, the presentation is asymptomatic. Alcoholic fatty liver in heavy alcohol drinkers have elevated liver enzyme levels with evidence of fatty changes on ultrasonographic or CT studies of the liver. Laboratory abnormalities are generally mild, and jaundice is unusual. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels may be elevated, but are usually lower than 300 IU/L. Patients with evidence of only hepatic steatosis on biopsy were perceived in the past to have a benign prognosis. However, a subset of patients with simple hepatic steatosis ean progress to fibrosis, or cimthosis in 10 years, especially ifthe drinking continues. Severity of steatosis, female sex, and the presence of giant mitochondria were independent predictors of disease progression." Management It includes abstinence from alcohol, life style modification and treatment for addiction management References 1. Dolores Morrison, Justine Sgrillo, and Lauren H. Daniels, Managing Alcoholic Liver diseases, 4 Lippincott Williams & Wilkins, 30, Nursing20141 November, available in: https://nursing.ceconnection.com/ovidfiles/00152193-201411000-00010.pdf 2. Mathurin P, Mendenhall CL, Carithers RL, et al. Corticosteroids improve short-term survival in patients with severe alcoholic hepatitis (AH): Individual data analysis of the last three randomized placcbo controlled double blind trials of cortict wvere AH. J Hepatol2002;36:480-487. 2) teroids in s 3. Carithers RL, McClain CJ. Alcoholic liver disease. In: Feldman M, Friedman LS, Brandt LJ, ed. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. Sth ed. St. Louis, MO: WB Saunders; 2016:1409-1427 unCHAPTER 3 Alcoholic Hepatitis Heavy alcohol ingestion leads to both acute and chronic liver diseases. The harmful use of alcohol has been estimated to cause approximately 3.3 million deaths every year, corresponding to nearly 6% of all deaths globally. Acute alcoholic hepatitis (AH) is a serious form of acute decompensation of alcoholic liver disease (ALD) that develops in heavy drinkers, National Institute of Alcohol Abuse and Alcoholism (NIAAA) provided a working, definition of AH that includes onset of jaundice within 60 days of heavy consumption (> 50 giday) of alcohol for a minimum of 6 months, a serum bilirubin > 3 mg/dL, an elevated AST (50-400 U/L), an AST:ALT ratio > 1.5, and no other obvious cause for hepatitis, Patho-physiology The cardinal symptom of Alcohol Hepatitis (AH) is liver inflammation, marked by dense neutrophilic infiltrates and prominent increases of inflammatory cytokines.2 Alcohol induces cell death in hepatocytes, leading to the telease of damage-associated molecular patterns (DAMPs) that potently activate the immune system. Even in the absence of significant liver fibrosis, AH can increase intra hepatic resistance leading to portal hypertension and associated complications. Clinical manifestations Clinical manifestations of AH may include jaundice, anorexia, fever, abdominal pain, and liver decompensations due to portal hypertension, Typically, laboratory studies will show moderately elevated transaminases (rarely >500 IU/L), with aspartate aminotransferase-to- alanine aminotransferase ratio greater than 1.5 Bilirubin is elevated in acute AH'(Mengfei Liu, M.D., Vijay H. Shah) Management Screening for AH should be performed in high-risk populations, such as those in alcohol rehabilitations clinies, or harmful drinkers. Benzodiazepines are considered the ‘gold standard’ treatment for Alcohol Withdrawals, given their efficacy for reducing both withdrawal symptoms and the risk of seizures and/or delirium tremens. Long-acting benzodiazepines (e.g. diazepam, chlordiazepoxide) provide more protection against seizures and delirium, but short and intermediate-acting benzodiazepines (e.g. lorazepam, oxazepam) are safer in elderly patients and those with hepatic dysfunction. Regardless of the severity, alcohol abstinence is the comerstone of therapy and early management. Glucocorticoids, are considered as the standard of care for severe AH Considering the potential risk of Wemicke’s encephalopathy, supplementation with B- complex vitamins is recommended. Other general approaches include treatment of hepatic encephalopathy (lactulose, rifaximin) and treatment of ascites (salt restriction). 2Nurses responsibilities Providing care for patients with AH can be cumbersome for nurses. Because a patient's clinical status can deteriorate very rapidly, vigilant nursing assessments and interventions are required along with thorough patient and family education, Regardless of the circumstances surrounding a patient’s AH the goal is to slow progression of the disease, manage signs and symptoms, and help the patient achieve the best possible quality of life. Goals of nursing care include: ‘© Demonstrate a non-judgmental caring and trusting relationship ‘+ Nursing assessment should incorporate physical examination, alcohol dependence, nutritional status, withdrawal symptoms and emergency conditions like such as ascites and hepatic encephalopathy ‘+ Rectifications of nutritional deficiencies and achieve the caloric goals ‘+ Administer medications and assist in surgical interventions and biopsy + Pain management ‘+ Enforce abstinence and relapse prevention through brief intervention ‘+ Nursing management is focused on increasing patient comfort; monitoring daily ‘weights, intake and output, and serum electrolytes; and preparing the patient for a possible paracentesis, + To promote effective breathing, positioning should be therapeutic ‘+ Administration of lactulose for to reduce serum ammonia levels. and closely monitor the patient for dehydration and electrolyte abnormalities during lactulose therapy ‘+ Watch for subtle changes in mentation, slurred speech, agitation, and abnormal involuntary movements, Assess the patient for disorientation and asterixis, ‘* Comprehensive nursing care should be planned for a patient in coma considering their hygienic, nutritional, elimination and treatment needs ‘+ Educate family and patient about the condition, need for alcohol abstinence, symptom identification, relapse prevention, nutrition and home care Conclusion Patients with AH may be stigmatized by healthcare providers and society. To preserve human dignity, nurses must remain objective when providing care and refrain from judging patients. To accomplish this, nurses can employ self-reflection strategies to explore and clarify values and to identify sources of potential bias that hinder patient care. 13References 1. Dolores Morrison, Justine Sgrillo, and Lauren H. Daniels, Managing Alcoholic Liver diseases, 4 Lippincott Williams & Wilkins, 30, Nursing2014 | November , available in: https://nursing.ceconnection.comvovidfiles/00152193-20141 1000-00010.pdf 2. Mathurin P, Mendenhall CL, Carithers RL, et al. Corticosteroids improve short-term survival in patients with severe alcoholic hepatitis (AH): Individual data analysis of the last three randomized placebo controlled double blind trials of cortict vere AH. J Hepatol2002;36:480-487. 2) teroids in s 3. Carithers RL, McClain CJ. Alcoholic liver disease, In: Feldman M, Friedman LS, Brandt LJ, ed. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. Sth ed. St. Louis, MO: WB Saunders; 2016:1409-1427 4CHAPTER 4 ALCOHOLIC CIRRHOSIS Alcoholic cirrhosis involves replacement of the normal hepatie parenchyma with extensive thick bands of fibrous tissue and regenerative nodules, which results in the elinieal manifestations of portal hypertension and liver failure!" Excessive chronic alcohol use can cause eral different types of chronic liver dist including alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. Further-more, use of excessive alcohol can contribute to liver damage in patients with other liver diseases, stuch hepatitis C, hemochromatosis, and those patients whohave fatty liver discase related to obesity. Chronic alcohol use can produce fibrosis in the absence of accompanying inflammation and/or necrosis, Fibrosis canbecenttilobular, pericellular, or periportal. When fibrosisreaches a certain degree, there is disruption of the normal liver architecture and replacement of liver cells byregenerative nodules. In alcoholic cirrhosis, the nodules are usually <3 mm in diameter; this form of citthosis is referred to as micronodular. With cessation of alcohol use, larger nodules may form, resulting in a mixed micro nodular and macronodular cirrhosis Signs and symptoms Right upper quadrant pain, Jaundice, weakness, peripheral edema, abdominal distension, ot symptoms of gastrointestinal bleeding, sich as hematemesis or melena. Physical examination findings Spider angiomata, palmar erythema, gynecomastia with hepatic decompensation, patients may develop ascites, peripheral edema, or hepatic encephalopathy. Other clinical manifestations include The development of jaundice or encephalopathy. The abrupt onset of anyof these complications may be the first event prompting the patient to seek medical attention. Other patientsmay be identified in the course of an evaluation of routine laboratory studies that are found to be abnormal On physical examination, the liver and spleen may be enlarged, with the liver edge being firm and nodular. Other frequent findings include Scleral icterus, palmar erythema, spider angiomas, parotid gland enlargement, digital clubbing, muscle wasting, or the development ofedema and ascites. Men may have decreased body hair. 15General Findings Jaundice Spider angioma ‘Nodular liver Splenomegaly Ascites Coput medusae Cruveilhier Baumgarten syndrome Palmar Erythema White Nails Hypertrophic osteoarthropathy/ Finger clubbing Dupuytren’s contracture Gynecomastia, loss of male hair pattern Hypogonadism Flapping tremor (asterixis) Foetor hepaticus Anorexia, fatigue, weight loss, muscle wasting Type 2 diabetes Description Yellow discoloration of skin, cornea and ‘mucous membranes Central arteriole with tiny radiating vessels, mainly on trunk and face Irregular, hard surface on palpation Enlarged on palpation or in ultrasound Proteinaceous fluid in abdominal cavity, clinically detected when 21.5 L Prominent veins radiating from umbilicus Epigastric vascular murmur Erythema sparing the central portion of the palm Horizontal white bands and/or proximal white nail plate Painful proliferative osteoarthropathy of long bones Fibrosis and contraction of the palmar fascia Benign proliferation of glandular male breast tissue Mainly in alcoholic cirrhosis and hemochromatosis ‘Asynchronous flapping motions of dorsiflexed hands ‘Sweet, pungent smelt Occurs in >50% of cirrhoties Occurs in 15-30% of cirrhoties 16 Etiology Compromised hepatocyte excretory function, occurs when serum bilirubin >2mg/dl Elevated estradiol, decreased estradiol degradation in liver Fibrosis, irregular regeneration Portal hypertension, splenic congestion Portal hypertension Portal hypertension, reopening of the umbilical vein that shunts blood from the portal vein Shunts from portal vein to umbilical vein branches, can be present without Caput medusae Elevated estradiol, decreased estradiol degradation in liver Hypoalbuminemia Hypoxemia due to right-to-left shunting, porto-pulmonary hypertension Enhanced oxidative stress, elevated hypoxanthine (alcohol ‘exposure or diabetes) Enhanced conversion of androstenedione to estrone and estradiol, decreased estradiol degradation in liver Direct toxic effect of alcohol or Hepatic encephalopathy, disinhibition of motor neurons Volatile dimethylsulfide, especially in portosystemic shunting and liver failure Catabolic metabolism by diseased liver, secondary to anorexia Disturbed glucose utilization ‘and/or decreased insulin removal by the liverClinical features + Cirrhosis can be diagnosed early without great effort or expense (identification of clinical risk constellations, physical examination, laboratory testing including complete blood count and liver function tests, ultrasonography), + Noninvasive testing is being increasingly used to detect hepatic fibrosis and to stage liver disease. Diagnosis The diagnosis of liver citrhosis is histologically characterized by fibrous septa between the portal fields; it comes in micro- and macronodular forms. The condition is diagnosed by its characteristic findings on clinical examination, laboratory tests, and ancillary studies. The typical findings in cirrhosis include, cutaneous signs of liver disease, a firm liver on palpation Liver Biopsy is considered the gold standard for diagnosis of cirmhosis, and sequential histological grading of inflammation arid staging of fibrosis can assess risk of progression Management Abstinence is the comerstone of therapy for patients with alcoholic liver disease. In addition, patients require good nutrition and long-term medical supervision in order to manage underlying complications that may develop. Complications such as the development of ascites and edema, variceal hemorrhage, or porto-systemic encephalopathy all require specific management and treatment. Glucocorticoids are occasionally used in patients with severe alcoholic hepatitis in the absence of infection. Survival has been shown to improve in certain studies. Treatment is restricted to patients with a discriminant function (DF) value of >32. The DF is calculated as the serum total bilirubin plus the difference in the patient's prothrombin time compared to control (in seconds) multiplied by 4.6, In patients for whom this value is >32, there is improved survival at 28 days with the use of glucocorticoids. Other therapies that have been used include oral Pentoxifylline, which decreases the production of ‘tumor necrosis factor a (TNF-) and other pro-inflammatory cytokines, In contrast to glucocorticoids, with which complications can occur, Pentoxifylline is relatively easy to administer and has few if any side effects. A variety of nutritional therapies have been tried with either parenteral or enteral feedings; however, itis unclear whether any of these modalities have significantly improved survival. Recent studies have used. parenterally administered inhibitors of TNF- such as Infliximab or Etanercept. Earlyresults have shown no adverse events; however, there was no clear-cut improvement in survival. Anabolic steroids, propylthiouracil, antioxidants, colchicine, and penicillamine have all been used but do not show clear-cut benefit and are not recommended. uvReferences Dolores Morrison, Justine Sgrillo, and Lauren H. Daniels, Managing Alcoholic Liver diseases, 4 Lippincott Williams & Wilkins, 30, Nursing2014 I November, available in: https://nursing.ceconnection.com/ovidfiles/00152193-201411000-00010.paf Mathurin P, Mendenhall CL, Carithers RL, et al. Corticosteroids improve short-term survival in patients with severe alcoholic hepatitis (AH): Individual data anal the last three randomized placebo controlled double blind trials of corticosteroids in severe AH. J Hepatol2002;36:480-487. 2) carithers RL, MeClain CJ. Alcoholic liver disease. In: Feld man M, Friedman LS Brandt LI, ed. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. Sth ed. St. Louis, MO: WB Saunders; 2016:1409-1427 sof 18Co. CHAPTER S mplications of Alcoholic Liver diseases 1. Variceal Hemorrhage ‘The presentation is usually with hematemesis or melena, Management options include end loscopic band ligation, sclerotherapy, and placement of transjugular intrahepatic portosystemic shunt placement (TIPS). TIPS increases the risk of hepatic encephalopathy. Ca uses Severe liver scarring (cirrhosis). A number of liver diseases — including hepatitis infection, alcoholic liver disease, fatty liver disease and a bile duct disorder called primary biliary cirrhosis — can result in cirrhosis, Blood clot (thrombosis). A blood clot in the portal vein or in a vein that feeds into the portal vein (splenic vein) can cause esophageal varices. Parasitic infection, Schistosomiasis is a parasitic infection found in parts of Afiica, South America, the Caribbean, the Middle East and East Asia, The parasite can damage the liver, as well as the lungs, intestine, bladder and other organs. Clinical manifestation, ‘+ Vomiting large amounts of blood + Black, tarry or bloody stools + Light headedness ‘© Loss of consciousness in severe cases ‘+ Yellow coloration of your skin and eyes (jaundice) ‘+ Easy bleeding or bruising ‘* Fluid build-up in your abdomen (ascites) Nursing responsibilities This ‘© Monitor Vital signs closely and assess level of consciousness frequently ‘© Observe for signs of hypovolemic shock. © Measure and record 1&0. * Administer IVF’s and blood, as ordered. ‘© Initiate balloon tamponade, as ordered. Assess the patient’s mental status and coping mechanisms, ‘© Reinforce teaching and explanations. 2. Ascites: s is the most common complication of alcoholic liver disease in which there is an accumulation of fluid in the peritoneal cavity. The patient usually presents with abdominal 19distension and pedal edema. It can be managed with sodium restriction, diuretics, paracentesis, and TIPS. Causes © Meigs syndrome © Vasculitis ‘Hypothyroidism «Renal dialysis ‘© Peritoneum mesothelioma + Abdominal tuberculosis * Mastocytosis Clinical manifestations + Weight gain ‘+ Shortness of breath, also called dyspnea. © Abdominal swelling, ‘Sense of fuliness or bloating + Sense of heaviness. + Indigestion. ‘+ Nausea or vomiting, ‘+ Changes to the belly button. Nursing responsibilities ‘+ Report decrease in fatigue and increased ability to participate in activities. ‘+ Maintain a positive nitrogen balance, no further loss of muscle mass, and meet nutritional requirements. ‘+ Decrease potential for pressure ulcer development and breaks in skin integrity, Reduce the risk of injury ‘© Verbalize feelings consistent with improvement of body image and self-esteem, ‘+ Increase level of comfort. ‘+ Restore normal fluid volume. ‘+ Improve mental status, maintain safety, and ability to cope with cognitive and behavioral changes. ‘+ Improve respiratory status. ‘+ Position bed for maximal respiratory efficiency; provide oxygen if needed, ‘+ Initiate efforts to prevent respiratory, circulatory, and vascular disturbances, ‘+ Encourage patient to incr exercise, 3. Spontaneous Bacterial Peritonitis (SBP) Itis an infection of ascitic fluid with no evidence of any other intraabdominal source (e.g. @ perforated viscus) of infection, The diagnosis can be confirmed by positive ascitic fluid 20