Alcoholic Liver Cirrhosis and Hepatic Encephalopathy

Major Clinical Case Study

February 8, 2011

Angela Boadu University of Maryland, College Park Dietetic Intern 2010-2011

Discussion Points
Executive Summary General Information Social History Medical/Surgical Data
Past Medical History Past Surgical History Admitting Physical Exam Diagnostic Tests Surgical Procedures Since Admission Laboratory Values

Nutritional History from Initial Encounter

Diet History Weight History Physical Activity Level Estimated Nutrient Needs Nutrition Care Process

Hospital Course
Medical and Nutritional Treatment

Medical Considerations Medical Nutrition Therapy References

Executive Summary
The liver is a 3-pound organ, consisting of a right lobe and left lobe, which the body depends on to provide metabolic and nutritional control. Alcoholic liver disease is a disease resulting from excessive alcohol ingestion. The pathogenesis of alcoholic liver disease progresses in three stages with the final stage being cirrhosis. Treatment of cirrhosis focuses on stopping the development of the scar tissue if possible and treating any complications.

Figure 1: A normal liver (left) showing no signs of scarring and a cirrhotic liver (right). (Source: Mayo Foundation for Medical Education and Research)

General Information
47-year-old Caucasian female with an extensive history of alcohol abuse Admitted with abdominal pain, slurred speech, drowsiness, and yellow-tinted whites of her eyes. Admission height: 5 7 (170 cm) Admission weight, following paracentesis of 6 liters of fluid: 142# (64.4kg); BMI=22.2; IBW 135# Dx: Hepatic Encephalopathy with Significant Ascites, and Alcoholic Liver Cirrhosis Date of admission: Wednesday, November 3, 2010 Date of discharge: Thursday, November 13, 2010

Social History
VM is a single mother of two sons, both serving in the Navy. She lives alone in a townhouse, with frequent visitations from her supportive significant other. Tobacco use is less than a half a pack a day. A distant history of spousal abuse was thought to be the cause of her heavy drinking.
Current amounts were not clearly described

Medical/Surgical Data

Past Medical History

Thyroid cancer (no recurrence) Hypothyroidism Liver disease Cirrhosis Rosacea GERD Anxiety Disorder Prior h/o type 2 diabetes and hypertension no longer require medication, but are diet controlled

Past Surgical History

Cervical excision and total thyroidectory Tonsillectomy Adenoidectomy Breast reduction surgery as a young adult

Admitting Physical Exam

Small-framed Vital signs were stable. Facial rosacea Abdomen was rounded and symmetric, positive bowel sounds x4 The patient did note pain inside her ribs and under her left breast, which is chronic but much improved after the paracentesis performed the morning of admission. Hemoccult positive stool in the emergency department

Diagnostic Tests
Abdominal x-ray suggestive of a small bowel obstruction (11/4/10) Pelvic ultrasound demonstrating a large amount of ascites (11/4/10) Computed tomography (CT) scan of the patients abdomen and pelvis demonstrating massive abdominal and pelvic ascites (11/6/10 )

Figure 3: CT (left) and Ultrasound (right) of Abdomen with loculated ascites (Source: Loyola University Health System Stritch School of Medicine)

Bowel loops float anteriorly.

Surgical Procedures Since Admission

Ultrasound-guided paracentesis performed
11/3/10 (PTA) 6 Liters 11/8/10 therapeutic 11/12/10 4.5 Liters

Laboratory Values
sodium = hyponatremia chloride = possible hypochloremia acidosis protein and albumin = hypoalbuminemia - decreased production of albumin contributing to ascites amylase and lipase = possible pancreatic damage ammonia = contributing to hepatic encephalopathy glucose = glucose intolerance WBC = infection hematologic values, specifically RBC, Hgb, Hct, MCV, MCH= macrocytic anemia due to chronic disease and hypovolemia (most likely due to fluid losses or decreased fluid intake) LFTS, specifically AST and Bilirubin (= jaundice) = liver disease

Nutritional History from Initial Encounter

Diet History
Balanced diet with minimal salty foods and sweets.
Canned and pre-packaged foods were purchased for convenience with patient not aware of high sodium content of some food items. Prior to acute onset of symptoms, patients appetite and intake had been good. Reported physician directives in hospital

Allergies? N Intake of vitamins, minerals, oral supplements, and/or health food store alternative supplements? N Cultural attitudes that influence dietary intake? N Past/present dietary/nutritional therapy? N

Weight History and Physical Activity Level

VM reported recent weight gain (secondary to fluid retention) with loss of visible body muscle. Limited physical activity, requiring a walker to get around the house New evening hours job limiting significant others ability to provide physical and emotional support for VM Mobility issues relate to reaching a bathroom on a different floor in the house

Nutrition Care Process

Initial Nutrition Diagnosis
NB-1.1 Food- and nutrition-knowledge deficit related to need for NAS diet (34 gm Na/low salt) of 1800 calories and nutritional supplement as evidenced by history of liver disease and current diagnosis of alcoholic liver cirrhosis.

Initial Nutrition Intervention

E-1.3 Education survival skills. Brief nutrition education to build and reinforce basic nutrition-related knowledge and provide essential nutrition information specific to management of liver cirrhosis.

Nutrition Monitoring
FH-1.1.1.1 Total energy intake. Assessment of food recall given by patient verifying adequacy of intake in the promotion of healthy weight gain Laboratory values. BD-1.2.5 Sodium. Criteria: 135-145 mmol/L BD 1.11.1 Prealbumin. Criteria: 18- 45 mg/dl (to evaluate visceral protein stores and adequacy of intake) May also want to monitor control of symptoms, such the reoccurrence of ascites

Hospital course
Day 1
Paracentesis Hyponatremia and hyperkalemia Ammonia levels Diet: 1800 calorie No Added Salt (NAS) diet (3-4 gm Na/low salt), and given the oral nutritional supplement Ensure Plus B.I.D. Limited intake reported. IV fluids: IV normal saline at 75 cc/hr

Day 2
Folic acid, thiamine, multivitamins IV normal saline was stopped due to concern on its impact on heart rate. Lactulose was held

Day 3
Possible spontaneous bacterial peritonitis Elevated finger sticks Possible acute renal failure/acute kidney injury Possible short bowel obstruction, either an ileus or mechanical obstruction Diet: NPO

Day 5
Diet: NPO except meds and ice chips with eventual transition to a clear liquid diet for evening meal

Hospital Course Continued

Day 6
Ascites re-accumulation, but minimal urinary output required some IV hydration Therapeutic paracentesis and IV albumin infusion GI status improved, and NG tube was removed Diet: NPO for procedure this morning, with orders for a soft diet thereafter.

Day 7
Lactulose was decreased, but pt still inconsistent in answers to questions. Diet: NPO

Day 8
Diet: Soft, NAS diet w/ percent intake of meals intake reported at 5%

Day 9
Hepatic encephalopathy was resolved on Rifaximin and Lactulose. Diet: Soft, NAS diet. Patients appetite fair w/ percent intake of meals noted at 25%

Day 10
Paracentesis Clostridium difficile colitis Liver transplant list Diet: Sodium restriction continued on Soft, NAS diet w/ percent intake of meals noted at 75%

Day 11
Patient discharged home Diet: Soft, NAS diet with percent intake of meals 100%

Estimated Nutrient Needs

BEE x 1.2-1.3 (hospitalized patient) = 1630-1765 kcal/day 0.8 1.0 g/kg/d (hospitalized patient, non-stress) = 51-64 g protein/day 20 25 ml/kg/d (hospitalized patient with ascites and sodium level below 128 mEq/L) = 1288-1610 mL fluid/day

Medical Considerations
Moderate to severe malnutrition is a common finding in patients with liver cirrhosis, and has a severe negative impact on a patients prognosis. Glucose intolerance occurs in almost of patients with cirrhosis, and 10% to 37% of patients will develop overt diabetes. Hepatorenal syndrome is a renal failure associated with severe liver disease without intrinsic kidney abnormalities Hyponatremia often occurs because of decreased ability to excrete water resulting from the persistent release of antidiuretic hormone, sodium losses via paracentesis, or overly sodium restriction. Portal hypertension, hypoalbuminemia, and renal retention of sodium and fluid contribute to fluid retention
Large-volume paracentesis Diuretic therapy: Spironolactone and Furosemide

Ammonia is a direct cerebral toxin. The main source of ammonia is its endogenous production by the gastrointestinal tract from the metabolism of protein, and from the degradation of bacteria and blood from gastrointestinal bleeding.
Lactulose and Rifaximin

Liver transplant

Medical Nutrition Therapy

Overall meal plan that is well balanced and includes fruits and vegetables, whole grains, lean meats, and low-fat diary products. Sodium-restricted diet. Liquid supplement taken by mouth or through a NG tube. Consumption of four to six meals Diets which include easy to digest forms of protein, such as legumes, poultry and fish Supplementation of vitamins and minerals is often necessary because of inadequate intake and altered metabolism and absorption Fluid intake is usually restricted to 1 to 1.5 L/day, depending on the severity of the ascites.

Implications of findings to the practice of dietetics

Critical thinking on the part of the nutrition expert is key to balance the therapy for different conditions. So while there are evidence-based guidelines provided in the Nutrition Care Manual and the Evidenced Analysis Library that provide a strong foundation for nutritional recommendations it is imperative to remember that the intuition and problem-solving skills of physicians and nutrition professionals are of utmost importance to provide patients with hepatic cirrhosis the most thought out, individualized care.

References
Calculations for nutrition assessment Diseases and Conditions of the Liver, Gallbladder, and Pancreas > Cirrhosis. American Dietetic Association Nutrition Care Manual. Source: Manual. http://www.nutritioncaremanual.org/content.cfm?ncm_content_id=81465. Retrieved November 30, 2010. http://www.nutritioncaremanual.org/content.cfm?ncm_content_id=81465. Cirrhosis. Medline Medical Encyclopedia. Source: http://www.nlm.nih.gov/medlineplus/cirrhosis.html http://www.nlm.nih.gov/medlineplus/cirrhosis.html Topic last reviewed: May 07, 2010. Retrieved: November 25, 2010. Cirrhosis - National Digestive Diseases Information Clearinghouse (NDDIC). Source: http://digestive.niddk.nih.gov/ddiseases/pubs/cirrhosis/#treatment. Posted: December 2008. Accessed: December 14, http://digestive.niddk.nih.gov/ddiseases/pubs/cirrhosis/#treatment. 2010. Disease Process Diseases and Conditions of the Liver, Gallbladder, and Pancreas > Cirrhosis. American Dietetic Association Nutrition Care Manual. Source: http://www.nutritioncaremanual.org/content.cfm?ncm_content_id=81451. Retrieved November 30, 2010. http://www.nutritioncaremanual.org/content.cfm?ncm_content_id=81451. Friedman, LS. (2010). Surgery in the Patient with Liver Disease. Trans Am Clin Climatol Assoc. 2010; 121, 121, 192205. Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917124/. Retrieved December 14, 2010. 192 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917124/. Lindsey, A. (2010). Profound hyponatremia in cirrhosis: a case report. Cases J. 2010; 3: 77. Source: report. 77. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2851673/?tool=pubmed. Published online March 23, 2010. Retrieved http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2851673/?tool=pubmed. December 14, 2010. Mahan, LK., Escott-Stump, S. (2008). Krauses Food & Nutrition Therapy, 12th Edition. St. Louis: EscottKrause Edition. Saunders Elsevier. pgs. 708-726. 708Sanyal, A. Mullen, K. Bass, N. (2010). The Treatment of Hepatic Encephalopathy in the Cirrhotic Patient. Sanyal, Encephalopathy Gastroenterol Hepatol (N Y). 2010 April; 6(4_Suppl): 112. Source: 1 12. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886485/#__secid3913169. Retrieved: December 14, 2010. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886485/#__secid3913169. Tabers Cyclopedic Medical Dictionary, 20th Edition. (2001). Philadelphia: F.A. Davis Company. Taber Davis Understanding Cirrhosis of the Liver Patient Center of the American Gastroenterological Association. Source: http://www.gastro.org/patient-center/digestive-conditions/cirrhosis-of-the-liver. Topic Last Reviewed: April 2008. http://www.gastro.org/patient- center/digestive- conditions/cirrhosis- of- theRetrieved November 26, 2010.

Questions ??