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Alcohol and the Liver. A Case Study. Leslie Anderson. Patient Background. SH was 42 y.o . Caucasian male, married with 2 children Smoked half a pack a day, drank a fifth of whiskey daily Admitted to LDSH for alcohol detox – 08/11 Family History significant for Polycystic Kidney Disease.
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Alcohol and the Liver A Case Study Leslie Anderson
Patient Background • SH was 42 y.o. Caucasian male, married with 2 children • Smoked half a pack a day, drank a fifth of whiskey daily • Admitted to LDSH for alcohol detox – 08/11 • Family History significant for Polycystic Kidney Disease
Past Medical History • Hypertension • Dyslipidemia • Polycystic kidney disease (recent diagnosis) • Lymph node resection • Alcohol abuse with previous evidence of alcoholic hepatitis
Hospital Events/Procedures • 11/2: SH admitted to ER • 11/3: Transferred to ICU; Intubated d/t respiratory distress • Plan to admit to psychiatric unit to assist in his alcohol detoxification
Alcohol and the Liver • The liver detoxifies 90% of ingested alcohol • Metabolism of alcohol is the main cause of liver damage • Alcoholic Liver Disease (ALD) is the cause of 50% of all liver disease cases • SteatosisSteatohepatitis Cirrhosis
Risk Factors • Binge/Chronic Drinking • Drinking between meals • Type of beverage • Family history of disease • Females > Males
Metabolism of Alcohol • Alcohol Dehydrogenase (ALD) • Metabolizes 80% of ingested alcohol • Ethanol AcetaldehydeAcetateAcetyl-CoACo2 +H2O • Leads to hepatic steatosis • Cytochrome P450 2E1 (CYP2E1) • Previously called inducible microsomal ethanol-oxidizing system (MEOS) • Used most in chronic alcoholism • Catalase enzyme • Non-oxidative process • Leads to hepatic steatosis
Toxic Effect of Alcohol • Ethanol • “Leaky gut” • Reactive Oxygen Species (ROS) • Compromised immunity • Acetaldehyde – Key toxin • Cellular damage, inflammation, extracellular matrix remodeling and fibrinogenesis • Acetate/Acetyl Co-A • Increased IL-6, IL-8, TNF-a • Effects perpetuate and progress
Nutritional Concerns • Malnutrition • Alcohol substitution • Malabsorption • Altered macronutrient metabolism • Reduced glucose production, often accompanied by insulin resistance • Lipids are malabsorbed and remain in circulation d/t decreased bile secretion • Increased protein catabolism with inadequate resynthesis
Vitamin/Mineral Deficiences • Decreased: • Intake of nutritious foods • Absorption • Storage • Increased Use: • Antioxidants • Metabolism of alcohol
Proposed Supplements • Milk Thistle (Silymaryin) • Safe, well-tolerated • No benefit noted • S-Adenyosylmethionine • Precursor to glutathione (antioxidant) • No benefit seen • Metadoxine • Not approved in U.S. • Decreased lipid accumulation • Phosphatidylcholine • Fibrosis-reducing effect • More studies needed
Anthropometrics • Wt: 106.3 kg • Ht: 182.9 cm • IBW: 80.8 kg • % IBW:132 • BMI: 31.78 • Adj BW: 90.5 kg
Estimated Nutrition Needs • 2100-2550 kcals (23-28 kcal/kg) • 80-95 g protein (1.0-1.2 g/kg) • 2800 ml fluid (35 ml/kg) • Adjusted wt used for energy needs • IBW used for protein and fluid needs
Clinical Data • Febrile – 38.9º C • Tremors – r/t alcohol detoxification • Questionable ascites • Unable to determine d/t body habitus
Medications • Anesthesia/Sedative • Propofol – (85 kcal/day) • Antianxiety • AntiGERD • Antiemetic • Fluid/Electrolyte/Vitamin replacement
Nutrition Assessment • Pt at high nutrition risk r/t inability to take PO, confusion, and intubation. BMI 31.8 indicates obesity. Albumin was wnl upon admit, with lowered labs d/t fluid administration. Altered labs r/t liver disease precipitated by alcohol consumption. Will continue to monitor lipase to determine possibility of PO intake vs. need for NJ past ligament of Trietz upon NPO day 2. Decreased estimated energy requirements d/t intubation. Unable to talk to pt at this time.
Nutrition Problem & Goals • Excessive alcohol intake r/t alcohol or drug addiction AEB elevated alcohol, LFT’s, and lipase lab values. • Advance diet as tolerated and as medically able.
Interventions • MVI, thiamin, folic acid • NPO d/t elevated lipase
Recommendations • If still NPO by tomorrow, recommend initiation of enteral feeds past the ligament of Trietz. Initiate feeds of Peptamen AF @ 20 ml/hr and monitor labs for refeeding syndrome as Phos is already low. End goal rate for pt is Peptamen AF @ 75 ml/hr = 24 kcal/kg Adj wt and 1.7 g prot/kg.
Prognosis • Poor d/t: • PKD • Alcoholic Hepatitis • continued alcohol abuse • Need for continued medical care • Possible dialysis • Possible transplants
References • Hasse JM, Matarese LE. Medical nutrition therapy for liver, biliary system, and exocrine pancreas disorders. In: Mahan LK, Escott-Stump S, ed. Krause’s Food & Nutrition Therapy. 12 ed. St. Louise, MO: Saunders Elsevier; 2008:707-727. • The Merck Manual of Diagnosis and Therapy. 18th ed. Whitehouse Station, NJ; 2006:1129-1131. • Seth D, Haber PS, Syn WK, Diehl AM, Day CP. Pathogenesis of alcohol-induced liver disease: classical concepts and recent advances. J GastroenterolHepatol. 2011:26;1089-1105. • Szabo G, Mandrekar P. Focus on: Alcohol and the liver. Alcohol Res Health. 2010:33;87-96. • Griffith CM, Schenker S. The role of nutritional therapy in alcoholic liver disease. Alcohol Res Health. 2006:29(4):296-306.