ALCOHOLIC LIVER DISEASE: CIRRHOSIS - Weebly

Wanyi Wang7varices) or stomach (gastric varices) rupture. Portal hypertension can also cause fluid toaccumulate in the legs (edema) and in the abdomen (ascites).The liver helps in making clotting factors or protein that coagulate the blood. So, when theliver is not producing these coagulation factors, you can get bruising easily.DiagnosisThe diagnosis of the alcoholic liver disease can be based on clinical and laboratory tests.The diagnostic tests include serum aspartate aminotransferase/alanine aminotransferase(AST/ALT). If the AST: ALT ratio is greater than 2, it can be utilized as an indicator that the liverdisease is associated with alcohol. The gamma-glutamytranspeptidase (GGT) can also be elevated[16]. In addition to the blood labs, ultrasonography to computed tomography imaging, magneticresonance imaging (MRI) tool is also utilized to detect for cirrhosis, as well as the signs of portalHTN. The most cost-effective choices might be the ultrasound compared to MRI and MRspectroscopy.Liver biopsy is considered the gold-standard diagnostic method to confirm the diagnosisand to determine the extent of the liver injury and the prognosis of cirrhosis. Biopsy helps rule outother coexisting conditions such as hepatitis C, hemochromatosis, or Wilson’s disease.Furthermore, according to a recent study of patients with alcoholic cirrhosis, early liver biopsy hasbeen very helpful in providing insights to help assess the stage of the liver disease[17].After liver disease or cirrhosis has been diagnosed, it’s essential to be able to assess theseverity of the disease in order to determine the best treatment plan and to predict the mortalityrate. Since 1978, the Maddrey discriminant function (DF) has been in use to help predict themortality rate of the disease. A DF value 32 is an indicator of a high -risk morality and the patientwill likely to be prescribed with corticosteroid therapy [16]. A more recent predictive model used7

Wanyi Wang8is Model for End-stage Liver Disease (MELD) score created by the Mayo Clinic, which involvesserum bilirubin, creatinine, and INR. Another clinical tool that has been widely used to determinethe diagnosis cirrhosis in the patient is the Child-Turcotte-Pugh (CTP), which is based on bilirubin,albumin, an International Normalized Ratio (INR), and grade of encephalopathy and ascites [16].TreatmentIt’s important to prevent continued liver damage by identifying the underlying cause andthe treatment. In the past cirrhosis was generally thought to be irreversible but recent studies haveshown that treatments aimed at the underlying cause especially in earlier stages of the disease canimprove or even reverse fibrosis [18]. Overall, the first line of treatment for cirrhosis is abstentionfrom alcohol and treating the underlining etiologies of cirrhosis.Ascites is the most common complication of cirrhosis. The mainstays of first-line treatmentof patients with cirrhosis and ascites include (1) education regarding dietary sodium restriction(2000 mg per day [88 mmol per day]) and (2) oral diuretics. More stringent dietary sodiumrestriction can speed mobilization of ascites but is not recommended because it is less palatableand may further worsen the malnutrition that is usually present in these patients. Fluid loss andweight change are directly related to sodium balance in patients with portal hypertension-relatedascites. It is sodium restriction, not a fluid restriction, which results in weight loss, as fluid followssodium passive. Oral diuretics (spironolactone and furosemide are commonly used) and nonsteroidal anti-inflammatory drugs (NSAIDs) can also be part of the treatment plan.Another complication of cirrhosis is GI bleeding, which is the second admission diagnosisfor case study patient A. Cirrhotic patient with GI bleeding should receive spontaneous bacterial8

Wanyi Wang9peritonitis (SBP) antibiotic prophylaxis combined with either intravenous or oral ceftriaxone for aperiod of 7 days to prevent infection in patients with variceal hemorrhage [19].In addition, hepatic encephalopathy, elevated ammonia level, accompanied with mentalconfusion, asterixis is another complication of cirrhosis. The neuropsychiatric disturbance that canbe corrected with the proper treatment. Lactulose, a non-absorbable disaccharide cathartic and/orwith Rifaximin therapy can help reduce the nitrogenous load in the gut, thus reduce the ammonialevel production. In a double-blind, randomized, controlled trial of lactulose (3 times per day andtitrated to produce 3 soft stools per day) with or without Rifaximin (400 mg 3 times per day) in120 patients with overt HE, this research studied found that mortality was reduced significantlywith combination therapy, which may be due to the antimicrobial properties of Rifaximin and theresulting lower rates of sepsis. So, Lactulose plus Rifaximin is superior to lactulose alone inreversing hepatic encephalopathy [18].If the cirrhosis has progressed to the end-stage and to the point that it could not function,then liver transplantation will be needed. Total counts of liver transplants in 2017 is 8,082according to the U.S. Department of Health & Human Services. And the number of livertransplants increased by 20.7% between 2007 and 2016 according to the data from OrganProcurement and Transplantation Network (OPTN) and Scientific Registry of TransplantRecipients (SRTR) 2016 Annual Data Report [20].Nutrition TherapyPatient with cirrhosis and alcoholic hepatitis have increased nutritional demands, but manyhave an average of daily intake of 50% of the recommended calorie intake. Acute Nutritionalintervention in cirrhotic patients should aim to support hepatic regeneration, prevent or correctmalnutrition and prevent and/or treat the complications associated with cirrhosis.9

Wanyi Wang10Despite alcohol having relatively higher kcal per gram (2.3-18 kcal/g) than carbohydrate(4.1 kcal/g) in average, patients are still observed with primary or secondary malnutrition. Acommon nutrition diagnosis for a patient with cirrhosis is protein-energy malnutrition orinadequate protein-energy intake. The contributing factors includes: (1) low dietary intake due toimbalanced diet pattern or replacement of food calories by the heavy alcohol consumption givingthe false conception that they are full; (2) poor appetite related to dysguesia, esophagitis, gastritis,and poor dental condition; (3) alteration in sense of taste and smell; (4) malabsorption of nutrientsecondary to diarrhea, nausea and vomiting, exogenous pancreatic insufficiency; (5) clinicalcomplications secondary to liver disease such as ascites, hepatic encephalopathy [22-24].Fat soluble vitamin deficiencies are common manifestations of malnutrition and liverdisease. Vitamin A (retinol) is implicated in ocular retinoid metabolism, tissue repair, andimmunity, and is principally stored in hepatic stellate cells. As stellate cells become activated, theylose their vitamin A stores and are then capable of producing collagen and subsequent fibrosisThe chronic liver disease commonly results in vitamin D deficiency. It was postulated thata key mechanism responsible for the low serum 25-hydroxy-vitamin D levels in patients with theend-stage liver disease may relate to the decreased hepatic production of vitamin D binding protein.Vitamin E deficiency has been well documented in alcoholic liver disease. However, the beneficialeffects of vitamin E supplementation in liver disease are dependent upon the nature of the disorder.For example, vitamin E supplementation in ambulatory patients with decompensated alcoholiccirrhosis was not beneficial at 1-year follow-up [25] .Deficiencies in pyridoxine (vitamin B6), folate (vitamin B9) and cobalamin (vitamin B12)may develop rapidly in chronic liver disease due to diminished hepatic storage. An original studyshowed that 80% of 70 chronic alcoholics that were admitted to a large U.S. urban hospital had10

Wanyi Wang11low serum folate levels, including 44% with serum folate levels in the severely deficient range. Ingeneral, the three main cause of the folate deficiency in the patient with ALD is reduced folateabsorption by the small intestine, Abnormal liver uptake and low folate storage, and increasedurinary folate excretion [1].Many works of literature such as the American Association for the Study of Liver Disease(AASLD) and American College of Gastroenterology (ACG) recommend nutritional therapy incirrhosis when the patient is undernourished and cannot meet the calculated daily nutritionaldemand of 35-40 kcal/kg and protein intake 1.2-1.5 kg/day. Also, small frequent meals areencouraged, emphasizing breakfast and nighttime snack ([23] [24] [27] [28]).Enteral is recommended as the route of administration considering the risk ofcomplications when given parentally[26, 27] according to the European Society of ClinicalNutrition and Metabolism (ESPEN). Some benefits of enteral nutrition have been shown inpatients with alcoholic hepatitis, malnourished patients with cirrhosis and patients with livertransplantation[28], where glycogen stores may be depleted after overnight fast and metabolicconditions resemble prolonged starvation in healthy individuals.Current ResearchThe intestinal dysbiosis is common in chronic liver disease and can induce inflammatoryresponses and mediate the collagen deposition in the liver. A research was conducted in 2017, toevaluate the probiotic Lactobacillus rhamnosus GG (LGG) for the treatment of liver fibrosis in amodel of chronic cholestatic liver disease in rats. Lactobacillus rhamnosus GG (LGG) is acommensal Gram-positive bacterium widely used as a probiotic strain because of its beneficialeffects on the intestinal barrier and inflammatory profile. This study suggests that LGG can be a11

Wanyi Wang12promising therapy for adjuvant treatment of hepatic fibrosis. There were 29 rats in the study, onegroup (n 17) have bile duct-ligated and another group (n 17), have sham-operated. Two groupare randomly assigned to receive the (LGG) or phosphate buffered saline for 14 days. Researchersfound the treatment with probiotic LGG was able to reduce liver fibrosis and hepatic geneexpression of IL-6 in cholestatic liver disease rats [29].Case study: Patient APatient A is a Hispanic 44-year-old and was readmitted to the ICU unit due to an alteredlevel of consciousness, acute GI bleeds with dark emesis, with nausea and vomiting for three days,as well as melena. According to the patient medical record, he was first admitted in January to thehospital for a GI bleed and a long history of heavy alcohol abuse, alcoholic liver cirrhosis. Duringthe recent admission, in a GI doctor consult, it was revealed the patient had a probable cirrhosis.The patient was employed and lived at home. After admission, the patient was NPO, exceptmedication for GI rest. Patient A was given octreotide drip IV therapy and later a Banana bag withmultivitamin, thiamine, folic acid and dextrose 5% 0.45% sodium chloride were infused to thepatient. The rationale behind ordering banana bags for these patients is relatively simple–alcoholics are likely to have nutritional deficiencies related to their dietary preferences for alcoholover nutrient-dense foods, putting them at risk for complications. Furthermore, the administrationof fluids is conventionally believed to help speed up sobriety. The patient also received a bloodtransfusion after proper screening and cross-matching due to the anemia as shown in Table 3. Afterthe EKG was done, Patient continued with amlodipine, Aldactone, hydromorphone, and Protonixas shown in table 1 with further details [29].12

Wanyi Wang13On day 2 of stay, the patient was advanced to a clear liquid. The banana bag IV wasdiscontinued and 0.45% sodium chloride was infused to the patient because patient’s condition hasstabilized.On Day 3, Patient A underwent esophagogastroduodenoscopy (EGD) with band ligationof varices per anesthesia and propofol. Patient A was then transferred to the recovery room unit ina stable condition. During the hospital stay, the patient was provided reality orientation andsupportive psychotherapy.On day 4 of stay, the nutrition department received a consult for Patient A at risk formalnutrition at level 2 and above, and nausea, vomiting, diarrhea greater than 3 days. Patient A’sBMI upon this hospital admission was 22 kg/m2 (Normal) [29], using his admission weight of 67.5kg (148.5 pounds) and 175.2 cm (68.9 inches). During the assessment the patient was unarousableand the nurse-reported patient was unable to consume the clear liquid due to mental status. Nursefurther reported that the patient has not had an episode of vomiting, diarrhea or constipation afterthe admission. The nutrition department diagnosed the patient with inadequate oral intake relatedto mental status as evidenced by the patient was not alert enough to consume the clear liquid dietas reported by the nurse. Later in the day, an NG placement was ordered to provide adequatenutrition intake. The nutrition department calculated the estimated energy needed by using MSJ x1.2-1.3 activity factor (25-30 kcal/kg). The patient’s energy needs were calculated out to be 18662022 kcal, protein with 0.8-1 gm/kg, a range of 54-67 gm. The patient’s fluid needs were based onthe RDA method of 1 mL of fluid/calorie range of estimated needs computed out to 1800-2000 ml.Therefore, an NG tube feeding formula, Jevity 1.5 kcal was selected because it peptidebased advanced formula with ingredients to help manage inflammation and promote GI tolerance.The goal rate of 60 ml/hr. was recommended to provide 1980 kcal, 269 gm carbohydrate, 83 gm13

Wanyi Wang14protein, free water 1003 ml, and meeting 132% of RDI. and meets 100% of estimated calorie needsand 100% of estimated protein needs. Although the tube feeding goal was at 60 ml/hr., the nutritiondepartment recommended starting the feeding at 20ml/hr. as tolerated then advance to the goal rate.The recommended nutrition therapy for the patient was discussed with the medical doctor whoagreed with the plan. The recommended tube feeding was started the next day. Lastly, thedepartment scheduled a follow-up assessment for 2 days later to assess patient’s tolerance of thetube feeding rate and formulate (Table 4).On the day of 6, during the follow-up visit, the tube feeding was discontinued, patient Ahad already started the GI soft diet and tolerated it well with no nausea, vomiting, diarrhea orchewing/ swallowing difficulty. The patient discharged from the hospital on day 7 of his stay.According to the physician discharge summary note, patient’s discharge diagnosis was: alcoholiccirrhosis of the liver without ascites, portal hypertension, gastric varices, dehydration, and severeprotein-calorie malnutrition. The condition upon discharge was hemodynamically stable andimproved and the recommended discharge diet was cardiac diet. In sum, Patient A went througha series of diet changes, He began with NPO, then, went from clear liquid to NG tube due to alteredin the level of mental status. After patient’s condition stabilized, the patient was on GI soft diet.The goal of the nutrition department in Patient A’s stay in the hospital was to improve his nutritionstatus and provide adequate oral nutrition intake to prevent or avoid further damage to the liver.Risk Associated in the Role of RDN in Patient CareAccording to the physician discharged summary note, one of the patient’s dischargediagnosis was severe protein-calorie malnutrition. However, upon the review of all the chart notessince the first admission in January until the recent admission, there was not a nutrition intervention14

Wanyi Wang15provided to improve the protein-calorie energy intake via supplementations. There was also nohistory of nutrition education provided to patient A documented in the chart notes. It would bebeneficial to the patient if the nutrition department communicates and collaborates with the doctorsto encourage nutrition education consult before patient gets discharged. In addition, the dietitiancan monitor all the nutritional related labs with emphasis on vitamins and mineral levels to ensurethe patient is not deficient in certain vitamins and minerals such as fat-soluble vitamins and vitaminB complex.In addition, the patient will be benefited if dietitian follows a standard nutrition assessmentguide when assessing the calorie and protein needed. According to the Morrison’s NutritionAssessment Guide, a patient with uncomplicated cirrhosis, the estimated energy need should rangefrom 30-35 kcal/kg (RMR x1.2-1.4), and estimated protein needs range from 1-1.2 g/kg., whereas,Patient’s A, the calculated estimated energy needs was at 25-30 g/kg and protein needs at 0.8-1.0g/kg. Thus, the estimated needs for Patient A was likely to be not enough to improve his nutritionstatus. Also, the guideline mentions the need to evaluate vitamin D and thiamine forsupplementation due to the decreased hepatic production of vitamin D binding protein anddepletion of liver thiamine stores. (Morrison Nutrition Assessment Guide 2014)15

Wanyi Wang16Supplementary MaterialFigure 1: The progression for alcoholic liver injury to steatosis with scarring, inflammation andarchitectural distortion leading to cirrhosis. As a complication of cirrhosis, hepatocellularcarcinoma may occur. However, only a minority of patients with alcoholic steatosis progress tosevere liver injury.16

Wanyi Wang17Figure 2: Hepatic metabolism of ethanol by enzymes ADH, CYP2E1 and catalase. Each enzymegenerates acetaldehyde, a toxic and mutagenic metabolite of ethanol. While ADH ismetabolically stable regardless of the alcohol challenge and catalase is irrelevant with respect toits role in hepatic alcohol degradation, CYP2E1 is inducible and contributes most toacetaldehyde production during heavy alcohol consumption.Table 1: Clinical features of hepatitis or chronic liver disease17

Wanyi Wang18Table 2: List of medication patient was on after admission.MedicationUsesAmlodipineLower the blood pressureby relaxing the bloodvessels so the heart doesnot have to pump as hard.The consumption of grapefruit juice mayslightly increase plasma concentrations ofamlodipine.AldactoneSpironolactone, is an oraldiuretic and is also used totreat low potassium levelsAvoid a diet high in salt. Too much salt willcause your body to retain water and can makethis medication less effective. Do not use saltsubstitutes or low-sodium milk products thatcontain potassium. These products could causeyour potassium levels to get too high while youare taking spironolactone.LactuloseAmmonia reducer andlaxativePotassiumUsed to treat or preventlow amountsof potassium in the blood.Upset stomach, nausea, vomiting, gas,or diarrhea may occur as side effects.Used to treat or preventsodium loss causedby dehydration, excessivesweating.Side effects: nausea, vomiting, stomach pain.ChlorideSodiumChloride18Drug/ Nutrition InteractionSide effects: nausea, vomiting, mild diarrhea

Wanyi Wang19Table 3: Laboratory valuesLaboratoryAssayReferenceRangeDay 1Day 2Day 3Day 4Day 5Day 6Day 7Day (L)(L)(L)(L)(L)(L)(L)Hemoglobin (L)(L)(L)(L)(L)(L)(L)107.6103.8104.4101.6104.

According to the CDC, chronic liver disease was ranked 9th as one of leading cause of death in California. Within the United State in 2015, there were 21,028 deaths attributed to alcoholic liver disease. Worldwide, there were 493,330 deaths related to liver cirrhosis in 2010 [30]. In a