Critical Care case Study: Nutritional Management in the care of Decompensated Cirrhosis and ascites

Transcription

1 Critical Care case Study: Nutritional Management in the care of Decompensated Cirrhosis and ascites Click Becky Schneider to edit Master subtitle style August 2012

2 Overview Decompensated cirrhosis (ETOH-related), Ascites Medical management of the disease Nutritional assessment and management Patient details Review of research article

3 Liver failure Pathophysiology Damage to hepatocytes Acute versus chronic Can result in encephalopathy Diagnostic Criteria Clinical presentation Labs Biopsy Physical examination MRI/CT Symptoms: Nausea/Vomiting, Jaundice, Abdominal Pain

4 Treatment Abstinence from ETOH Fluid and nutrient provision Specific to symptoms: Varices/GI bleeding Ascites Peritonitis Hepatic encephalopathy

5 Nutritional implications Causes of nutrition-related problems Inadequate intake: early satiety (ascites), dietary restriction, ETOH in place of food, hospitalizations Decreased absorption Altered metabolism Consequences Weight loss Protein-calorie malnutrition Vitamin deficiencies (thiamin, folate, riboflavin (B2), pyridoxine (B6), ascorbic acid, vitamin A, v)

6 Nutritional Assessment Weight status: possible loss, fluid-related gains Recent intake UUN balance Fecal fat Temporal or upper extremity wasting Medications: Diuretics, Lactulose

7 Nutrition intervention Diet: Small, frequent meals/snacks rich in carbohydrate and high in calories Protein: Restriction only indicated in refractory hepatic encephalopathy Micronutrient supplementation- necessary in patients with alcohol-related cirrhosis (B vitamins, fat-soluble vitamins, Zinc, Selenium)

8 Case study patient Background o 80 year-old male; retired mechanic o Hx of heavy ETOH use o Past hx of smoking (quit in 1978) o Supportive family o No known recent weight loss

9 Anthropometrics Height: 193 cm (8/5) Weight: 110 kg (8/8) Weight: 116 kg UBW: 104 kg BMI: 29.4 IBW: 92 kg (120%)

10 Current condition Diagnosed with decompensated cirrhosis, ascites, AKI, lactic acidosis, and suspected COPD Unable to take PO for one week prior to admission due to abdominal pain, nausea, and vomiting Upon admission, hypotensive Received IVFs

11 Past medical history Heavy ETOH usage (15 beers/day) Diabetes Hypertension Hyperlipidemia PVD

12 treatment Receiving Lactulose, IV Fluids, insulin Paracentesis- 3 L removed Counsel to discontinue ETOH use Advance to Low Na diet

13 Assessment of nutrition-related problems Weight history, interview Lab values Estimation of energy and protein needs: EEN: kcal/d (20-23 kcal/kg) Protein: g/d ( g/kg IBW) Fluids: Per MD

14 intervention Supplement to attempt to meet protein needs Rally pack Labs: B12, Homocysteine, Folate, HbA1C, TGs Recommendation for long-acting diabetic medications when medically feasible Recommendation for meds- Reglan, Ursodiol

15 Monitoring/evaluation Supplement acceptance Preferences/menu choices Labs/medical progress Future: Calorie count to confirm inadequate PO Monitor need for initiation of enteral nutrition as patient has had minimal intake for over 1 week

16 Review of research article Body composition, muscle function, and energy expenditure in patients with liver cirrhosis: a comprehensive study Investigated the nutritional status and metabolic activity of 286 patients with cirrhosis. Measurements: resting energy expenditure with indirect calorimetry, total body protein by neutron activation analysis, and total body fat and bone mineral content by dual-energy X-ray absorptiometry, respiratory muscle strength with a pressure transducer and grip strength by dynamometry, dietary intakes of energy and protein

17 Research review continued 51% of the patients had significant protein depletion (P < ) (63% of mean and 28% of women) Increasing disease severity => prevalence of protein depletion also significantly increased (P < ) While protein depletion was associated with decreased function of muscle, it was not associated with lower protein and energy intake Loss of body protein- most common in alcoholic cirrhosis Hypermetabolism- in 15% of the patients; not associated with origin or severity of disease, sex, ascites, protein depletion, or presence of tumor

18 References Endoscopic Retrograde Cholangiopancreatography. Thomas Jefferson University Hospitals Accessed from: US:official&biw=1366&bih=664&tbm=isch&prmd=imvns&tbnid=GvRwNiAu8_y4EM:&imgrefurl= ospital.org/tests-and-treatments/endoscopic-retrograde cholangiopancreatography.aspx&docid=azr1q4xhs2eem&imgurl= 2.GIF&w=530&h=390&ei=SxooUKawFOSK6QHyl4BQ&zoom=1 ASPEN Manual The A.S.P.E.N. Nutrition Support Core Curriculul: Liver Disease. pp Gunter, J.A. and Barton, E.D. Cirrhosis WebMD, Inc. Accessed from: Acute Liver Failure Mayo Foundation for Medical Education and Research. Accessed from: Parrish, C.R Nutrition for Patients with Hepatic Failure. Practical Gastroenterology, Nutrition Issues in Gastroenterology, Series #6. Heidelbaugh, J.J. and Sherbondy, M. Cirrhosis and Chronic Liver Failure: Diagnosis and Evaluation Am Fam Physician, 74(5): Menachery, J. and Duseja, A. Treatment of Decompensated Alcoholic Liver Disease International Journal of Hepatology, doi: /2011/ Accessed from: Moore, K.P. Guidelines on the management of ascites in cirrhosis GUT, 55(suppl 6):vi1-vi12 doi: /gut Accessed from: Heidelbaugh, J.J. and Sherbondy, M. Cirrhosis and Chronic Liver Failure: Treatment and Complications Am Fam Physician, 74(5): O Brien, A. and Williams, R. Nutrition in End-Stage Liver Disease: Principles and Practice Gastroenterology, 134: doi: /j.gastro Marchesini, G. et al. Branched-Chain Amino Acid Supplementation in Patients with Liver Diseases The Journal of Nutrition, 135(6): Accessed from: