case study hepatic encephalopathy n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Case Study Hepatic Encephalopathy PowerPoint Presentation
Download Presentation
Case Study Hepatic Encephalopathy

Loading in 2 Seconds...

play fullscreen
1 / 62

Case Study Hepatic Encephalopathy - PowerPoint PPT Presentation


  • 701 Views
  • Uploaded on

Case Study Hepatic Encephalopathy. By: Cynthia Topley, MS Meredith College Dietetic Intern February 17, 2013. Overview. Introduction to Hepatic Encephalopathy (HE) Literature Reviews (3): Branched Chain Amino Acids (BCAAs), Lactulose, and Rifaximin Case Study Discussion Questions.

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

Case Study Hepatic Encephalopathy


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
    Presentation Transcript
    1. Case StudyHepatic Encephalopathy By: Cynthia Topley, MS Meredith College Dietetic Intern February 17, 2013

    2. Overview • Introduction to Hepatic Encephalopathy (HE) • Literature Reviews (3): Branched Chain Amino Acids (BCAAs), Lactulose, and Rifaximin • Case Study • Discussion • Questions

    3. Introduction to HE

    4. Definition HE occurs during liver failure. When this happens, the liver is unable to remove toxic substances - especially ammonia - from the bloodstream. Cognitive decline can result from increased ammonia within the bloodstream. Medlineplus Encyclopedia. Hepatic encephalopathy. http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm. Accessed December 4, 2013.

    5. Causes • Cirrhosis and hepatitis are leading causes of HE. • The liver metabolizes potentially harmful substances like alcohol or medications into nontoxic components. • When the liver is injured and unable to perform this task, toxic substances may build up within the gut, blood, and brain, which may cause HE. Medlineplus Encyclopedia. Hepatic encephalopathy. http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm. Accessed December 4, 2013.

    6. Causes, continued • Bacteria within the colon breakdown protein (from the diet) and produce ammonia. • Normally, ammonia is metabolized by the liver into urea and excreted out by the kidneys. • When this doesn’t happen, ammonia can build up in the blood and brain. • Ammonia is a neurotoxin itself but can also cause brain swelling. Brain swelling disrupts the transmission of signals from one neuron to another which can alter mental status. Morgan, M., Stubbs, M. Hepatic Encephalopathy in Patients with Cirrhosis. Gastroenterology. 2010;29(4):91-104. Medlineplus Encyclopedia. Hepatic encephalopathy. http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm. Accessed December 4, 2013.

    7. Symptoms May include: Disorientation, difficulty concentrating, making decisions or thinking, difficulty with writing and speaking, hallucinations Additional Symptoms of Liver Failure May Include: Jaundice, Ascites Medlineplus Encyclopedia. Hepatic encephalopathy. http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm. Accessed December 4, 2013.

    8. Tests Some tests to determine HE may include: • Liver function tests • Serum ammonia levels • BUN and creatinine to evaluate kidney function • MRI/CT of Head/Brain Medlineplus Encyclopedia. Hepatic encephalopathy. http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm. Accessed December 4, 2013.

    9. Stages Hepatic encephalopathy in patients with cirrhosis. Morgan, Marsha, Stubbs, Matthew. Gastroenterology. 2010;29(4):91-104.

    10. Treatment • HE is a serious condition. • Treatments usually involve halting the causes of HE. • As we know, HE may be exacerbated by protein degradation by colonic bacteria and accumulation of ammonia within the blood/brain, liver failure, and/or kidney failure. • Some patients need enteral or parenteral nutrition. Medlineplus Encyclopedia. Hepatic encephalopathy. http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm. Accessed December 4, 2013.

    11. Treatment, continued • Lactulose is a laxative. Lactulose is degraded by bacteria in the colon. This process inhibits release of ammonia into the bloodstream because the bacteria actually utilize ammonia for their own protein metabolism. The bacteria is then removed from the body via stools. • Rifaximin is an antibiotic. Antibiotics kill gut bacteria therefore decreasing the amount of bacteria producing ammonia and improving HE. Medlineplus Encyclopedia. Hepatic encephalopathy. http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm. Accessed December 4, 2013.

    12. Prognosis • Varies for each indiviudal • HE may be acute or chronic • HE may advance to coma and sometimes death Medlineplus Encyclopedia. Hepatic encephalopathy. http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm. Accessed December 4, 2013.

    13. Nutrients Impaired • May Include: • Fat soluble vitamins A, D, E, K - related to impaired hepatic bile excretion • B1 (thiamine), B3 (niacin), B6 (pyridoxine), B12, B9 (folate) - related to decreased intake, important in CHO metabolism • Iron - related to bleeding • Magnesium, Phosphorus, Zinc - related to increased excretion, diuretics Mahan, L, Escott-Stump, S., Raymond, J. Krause’s Food and the Nutrition Care Process. Edition 13. St. Louis, Missouri: Elsevier;2012.

    14. Nutrition Recommendations for HE O’Brien, A., Williams, R. Nutrition in End-Stage Liver Disease: Principles and Practice. Gastroenterology. 2008;134:1729-1740 Plauth, M., Cabre, E., Riggio, O., Assis-Camilo, M., Pirlich, M., Kondrum, J. Ferenci, P., Holm, E., vom Dahl, S., Muller, MJ., Nolte, W. ESPEN Guidelines on Enteral Nutrition: Liver disease. Clinical Nutrition. (2006) 25, 285-294.

    15. Literature Reviews

    16. Literature Review #1 Les, Iñigo; Doval, Eduardo; García-Martínez, Rita; Planas, Mercè; Cárdenas, Guillermo; Gómez, Pilar; Flavià, Montse; Jacas, Carlos; Mínguez, Beatriz; Vergara, Mercedes; Soriano, Germán; Vila, Carmen; Esteban, Rafael; Córdoba, Juan. Effects of Branched-Chain Amino Acids Supplementation in Patients With Cirrhosis and a Previous Episode of Hepatic Encephalopathy: A Randomized Study. American Journal of Gastroenterology. Jun2011, Vol. 106 Issue 6, p1081-1088.

    17. Introduction • Branched chain amino acids are necessary proteins obtained from dietary sources. • Leucine, isoleucine, valine • BCAAs may help treating HE by reducing ammonia levels • Mechanism still under investigation • BCAAs build up muscle proteins • Muscles are created by utilizing nitrogen • Nitrogen is found in ammonia, therefore BCAAs decrease ammonia levels when building muscle proteins The goal of this study was to explore how BCAA supplementation (30 g/day) may impact the return of HE in patients with a prior episode of HE. Les, Iñigo; Doval, Eduardo; García-Martínez, Rita; Planas, Mercè; Cárdenas, Guillermo; Gómez, Pilar; Flavià, Montse; Jacas, Carlos; Mínguez, Beatriz; Vergara, Mercedes; Soriano, Germán; Vila, Carmen; Esteban, Rafael; Córdoba, Juan. Effects of Branched-Chain Amino Acids Supplementation in Patients With Cirrhosis and a Previous Episode of Hepatic Encephalopathy: A Randomized Study. American Journal of Gastroenterology. Jun2011, Vol. 106 Issue 6, p1081-1088.

    18. Methods • Randomized, double-blinded study performed at 4 hospitals • 116 patients with cirrhosis • January 2003 – December 2008 • Standard diet 35 kcal/kg and 0.7 g pro/kg/day plus BCAA supplement (30 g/day) or maltodextrin supplement (30 g/day) for 56 weeks • Hypothesized a reduction in HE event by 25-50% with BCAAs • Nutritional assessments/dietary compliance performed by dietitians, psychologists evaluated HEs Les, Iñigo; Doval, Eduardo; García-Martínez, Rita; Planas, Mercè; Cárdenas, Guillermo; Gómez, Pilar; Flavià, Montse; Jacas, Carlos; Mínguez, Beatriz; Vergara, Mercedes; Soriano, Germán; Vila, Carmen; Esteban, Rafael; Córdoba, Juan. Effects of Branched-Chain Amino Acids Supplementation in Patients With Cirrhosis and a Previous Episode of Hepatic Encephalopathy: A Randomized Study. American Journal of Gastroenterology. Jun2011, Vol. 106 Issue 6, p1081-1088.

    19. Results • HE recurred in both groups (BCAA = 24, Maltodextrin = 32, P=.137) • Therefore, no significant reduction in HE occurance in BCAA group Les, Iñigo; Doval, Eduardo; García-Martínez, Rita; Planas, Mercè; Cárdenas, Guillermo; Gómez, Pilar; Flavià, Montse; Jacas, Carlos; Mínguez, Beatriz; Vergara, Mercedes; Soriano, Germán; Vila, Carmen; Esteban, Rafael; Córdoba, Juan. Effects of Branched-Chain Amino Acids Supplementation in Patients With Cirrhosis and a Previous Episode of Hepatic Encephalopathy: A Randomized Study. American Journal of Gastroenterology. Jun2011, Vol. 106 Issue 6, p1081-1088.

    20. Conclusion BCAA supplementation did not reduce the risk of developing HE in patients with a prior episode of HE. Discussion • Study did not differentiate between the type of protein a patient was consuming – animal versus plant • Further exploration behind the study design to use patients with prior episodes of HE versus no prior episodes of HE Les, Iñigo; Doval, Eduardo; García-Martínez, Rita; Planas, Mercè; Cárdenas, Guillermo; Gómez, Pilar; Flavià, Montse; Jacas, Carlos; Mínguez, Beatriz; Vergara, Mercedes; Soriano, Germán; Vila, Carmen; Esteban, Rafael; Córdoba, Juan. Effects of Branched-Chain Amino Acids Supplementation in Patients With Cirrhosis and a Previous Episode of Hepatic Encephalopathy: A Randomized Study. American Journal of Gastroenterology. Jun2011, Vol. 106 Issue 6, p1081-1088.

    21. Literature Review #2 Praveen Sharma, BarjeshChander Sharma, AmitAgrawal and Shiv Kumar Sarin.Primary prophylaxis of overt hepatic encephalopathy in patients with cirrhosis: An open labeled randomized controlled trial of lactulose versus no lactulose.Journal of Gastroenterology and Hepatology 27 (2012) 1329–1335.

    22. Introduction • Lactulose is degraded by colonic bacteria which utilize nitrogen (from ammonia) within the gut to build their own proteins. • Lactulose, therefore, improves HE by reducing serum ammonia levels. • The goal of this study was to explore whether or not lactulose could prevent HE in patients without prior history of HE. Praveen Sharma, Barjesh Chander Sharma, Amit Agrawal and Shiv Kumar Sarin. Primary prophylaxis of overt hepatic encephalopathy in patients with cirrhosis: An open labeled randomized controlled trial of lactulose versus no lactulose. Journal of Gastroenterology and Hepatology 27 (2012) 1329–1335.

    23. Methods • Randomized, controlled trial • 120 patients with cirrhosis (60 patients – lactulose 30-60 ml BID or TID to produce 2-3 stools/day, 60 patients – no lactulose) • Not blinded • January 2008 - September 2009 • Psychological testing was performed, patients evaluated each month for HE development Praveen Sharma, Barjesh Chander Sharma, Amit Agrawal and Shiv Kumar Sarin. Primary prophylaxis of overt hepatic encephalopathy in patients with cirrhosis: An open labeled randomized controlled trial of lactulose versus no lactulose. Journal of Gastroenterology and Hepatology 27 (2012) 1329–1335.

    24. Results • Incidence of HE lower in patients receiving lactulose • 11% of lactulose group developed HE compared with 28% in no-lactose group Conclusion Lactulose was found to be effective for primary prevention of HE in patients with cirrhosis. Praveen Sharma, Barjesh Chander Sharma, Amit Agrawal and Shiv Kumar Sarin. Primary prophylaxis of overt hepatic encephalopathy in patients with cirrhosis: An open labeled randomized controlled trial of lactulose versus no lactulose. Journal of Gastroenterology and Hepatology 27 (2012) 1329–1335.

    25. Discussion • Not blinded (lactulose dosed for 2-3 stools/day) • Did not address markers to indicate when lactulose therapy should begin among cirrhotic patients Praveen Sharma, Barjesh Chander Sharma, Amit Agrawal and Shiv Kumar Sarin. Primary prophylaxis of overt hepatic encephalopathy in patients with cirrhosis: An open labeled randomized controlled trial of lactulose versus no lactulose. Journal of Gastroenterology and Hepatology 27 (2012) 1329–1335.

    26. Literature Review #3 Bass, N., Mullen, K., Sanyal A., Poordad, F., Neff, G., Leevy, C., Sigal, S., Sheikh, M., Beavers, K., Frederick, T., Teperman, L., Hillebrand, D., Huang, S., Merchant, K., Shaw, A., Bortey, E., Forbes, W. Rifaximin Treatment in Hepatic Encephalopathy. New England Journal of Medicine.  362;12. March 25, 2010.

    27. Introduction • Rifaximin is a broad spectrum antibiotic. • May be used in treating HE because it kills ammonia-creating gut bacteria. • May be safer than other antibiotics because it is minimally absorbed. • The goal of this study was to explore the safety and effectiveness of using rifaximin to treat cirrhotic. patients with reccurent HE with rifaximin. Bass, N., Mullen, K., Sanyal A., Poordad, F., Neff, G., Leevy, C., Sigal, S., Sheikh, M., Beavers, K., Frederick, T., Teperman, L., Hillebrand, D., Huang, S., Merchant, K., Shaw, A., Bortey, E., Forbes, W. Rifaximin Treatment in Hepatic Encephalopathy. New England Journal of Medicine.  362;12. March 25, 2010.

    28. Methods • Randomized, double-blind, placebo-controlled study • 299 patients in HE remission were randomly assigned to a Rifaximin group (550 mg BID, 140 patients) or Placebo group (159 patients) for 6 months. Bass, N., Mullen, K., Sanyal A., Poordad, F., Neff, G., Leevy, C., Sigal, S., Sheikh, M., Beavers, K., Frederick, T., Teperman, L., Hillebrand, D., Huang, S., Merchant, K., Shaw, A., Bortey, E., Forbes, W. Rifaximin Treatment in Hepatic Encephalopathy. New England Journal of Medicine.  362;12. March 25, 2010.

    29. Results • Rifaximin reduced the risk of HE compared with the placebo • ~22% of patients in the Rifaximin group had an episode of HE compared with ~46% of patients in the placebo group • ~14% of Rifaximin patients needed hospitalization compared with ~23% of Placebo patients • Almost all patients received lactulose therapy Conclusion • Rifaximin significantly reduced the risk of developing HE compared with placebo Bass, N., Mullen, K., Sanyal A., Poordad, F., Neff, G., Leevy, C., Sigal, S., Sheikh, M., Beavers, K., Frederick, T., Teperman, L., Hillebrand, D., Huang, S., Merchant, K., Shaw, A., Bortey, E., Forbes, W. Rifaximin Treatment in Hepatic Encephalopathy. New England Journal of Medicine.  362;12. March 25, 2010.

    30. Discussion • Strong study overall • Explored preventative style of treatment with rifaximin as opposed to treatment after symptoms develop • Further explore specific relationship between rifaximin and lactulose . Bass, N., Mullen, K., Sanyal A., Poordad, F., Neff, G., Leevy, C., Sigal, S., Sheikh, M., Beavers, K., Frederick, T., Teperman, L., Hillebrand, D., Huang, S., Merchant, K., Shaw, A., Bortey, E., Forbes, W. Rifaximin Treatment in Hepatic Encephalopathy. New England Journal of Medicine.  362;12. March 25, 2010.

    31. Overall Conclusions • Evidence supports lactulose and rifaximin to prevent/treat HE. • Not enough evidence to support BCAAs to prevent/treat HE. Studies are conflicting so more research needs to be conducted.

    32. Case Study

    33. Case Study I. Personal History II. Medical History III. Nutritional History V. Food/Drug Interactions IV. Nutrition Assessment and Care Plan

    34. I Personal History

    35. I Personal History JY is a 58 year old female Two sisters JY moved in with sister 3 months ago due to disability from MVA No smoking, alcohol, or illicit drug use No religious affiliation, white not Hispanic background. Single, no kids Liberty Home Health assists the family

    36. II Medical History

    37. Past Medical History • Cirrhosis 2/2 hepatitis C with ascites, h/o encephalopathy • Portal hypertensive gastropathy, GI bleeding • ?seizure disorder. No recent seizures • Hypertension • Hyperlipidemia • Right leg cellulitis, ?vancomycin-resistant • Chronic low back pain following MVA • Obesity • Depression • Asthma

    38. History of Present Illness • On 10/25, sister called 911 because JY was increasingly confused, spent the day in bed, and presumed to have stopped taking her medications, including lactulose. • JY admitted to WakeMed - ? Transfer to UNC Liver Transplant Division when available bed. • Upon admission, JY with ammonia level >100 (nl 15-60 mg/dL), UTI, and right leg cellulitis.

    39. History of Present Illness, continued • JY with anemia from ongoing GI blood loss and worsening acute on chronic renal failure • JY was given lactulose (2 stools), rocephin, and 1 L fluid with some improvement in mental status per sister • JY hospitalized 09/30 -10/07 at UNC for right leg cellulitis • Cirrhosis 2/2 hepatitis C • Pt on waiting list for liver transplant at UNC

    40. Review of Systems on Admission 10/25/13 Normal unless otherwise specified. General: Unsteady on feet. Alert and oriented to herself, sister, and hospital but not to day, date, time, or season. Jaundiced with asterixis. Musculoskeletal: Low back pain. Heart:Tachycardic Abdomen: Significantly distended with ascites, but soft, tender, normal bowel sounds Extremities: 2-3+ pitting edema of bilateral extremities

    41. Impression on Admission 10/25/13 • Altered mentation, encephalopathic, probably multifactorial. • Negative Head CT, positive for asterixis, not taking lactulose with high ammonia level, consistent with HE. Currently with cellulitis and UTI - possibility of an infection worsening HE.

    42. Plan on Admission 10/25 • Reinstitute lactulose, monitor, and repeat electrolytes in the a.m. • Monitor liver enzymes. • Antibiotics include clindamycin for cellulitis and rocephin for UTI. • Hospitalist discussed at length why she was so hesitant to come to hospital and that she may be tiring of intervention but JY decided to comply with physician’s wish for hospitalization (Dr. M). • 1 L NS bolus in ED and received 1 unit packed RBC transfusion for low hemoglobin • GI consult

    43. Gastrointestinal (GI) Consult on Admission 10/25/13 • Reason: HE and acute renal failure with hepatitis C liver cirrhosis. Worsening renal function and persistent HE • RT nostril NGT placement • GI reports negative evaluation at UNC for hepatocellular carcinoma • ROS: Normal unless otherwise specified • Jaundiced, confused, obese with edema, unable to evaluate hepatosplenomegalybecause of body habitus. Lower extremities with 3+ pitting edema R>L. Redness and swelling RLE

    44. Gastrointestinal Consult, continued Labs: Na 145, K 3.5, Cl 117, Bun 47, Cr 3.82, ammonia 83, AST 60, ALT 17, tot bilirubin 5.5 Assessment: Worsening cirrhosis manifesting as encephalopathy. Liver insufficiency with elevated total bilirubin, HE and ascites. Acute on chronic renal insufficiency. RLE cellulitis. Plan: IV albumin 25 g 25% albumin TID (to increase intravascular volume). Increase lactulose to 30 g q3h until improved mental status. Continue rifaximin for HE. IV D5W with 150 mg bicarb drip @ 100 ml/hr for acidosis. Discuss pt’s status with Dr. Z, UNC Transplant Clinic. Nephrology consult

    45. Nephrology Consult on 10/28/13 • Reports worsening creatinine from 3.29 on admission to 3.86 current • Mental status improving but not 100% coherent • Currently no urine output, pt in diapers • NGT but NPO • Physical Exam: Normal unless otherwise specified • Respiratory: Decreased air entry bilaterally. GI: Abd soft, mildly tender. + bowel sounds. Extremities: 3+ pitting edema bilateral LE. • Neurologic: Extremely weak and difficulty moving extremities.

    46. Nephrology Consult, continued • Labs: Na 146, K 3.2, Cl 115, Bun 49, Cr 3.86, Glu 144, Total Bilirubin 4.0, Ammonia 83 • Assessment: • 1. Acute renal failure. Not responding to IV hydration and fluid bolus with worsening renal failure. Pt anasarcic*. • 2.Hypernatremia d/t NPO status • 3.Hypokalemia d/t NPO status and lactulose with multiple BMs • 4.Cirrhosis 2/2 hep C and worsening liver failure. • 5.Ascites • 6. Acidosis • 7. Edema of LE

    47. Nephrology Consult, continued • Plan: D/c IV fluid and start water flush 250 ml q 6 hr via NGT. Begin bicarb 1300 mg PO BID. Continue albumin replacement per GI recommendation. Give Lasix 40 mg IV. Insert Foley. Transfer to UNC when possible. Prognosis poor. Perform urinalysis. Discuss plan of care with sister. • Infectious Disease consult.

    48. Infectious Disease Consult on 10/28/13 • Currently IV rocephin and clindamycin. Additional meds include: albumin, Advair, lactulose, rifaximin, Zofran, and Ultram • Physical Examination: Normal unless otherwise specified. • Chest: Decreased air entry bilaterally due to poor inspiratory effort. Abdomen: Soft, distended with fluid. Nontender. Bowel sounds scant. Bilateral pitting edema LE. Neurological: Difficulty moving extremities. • Assessment & Plan: Mild erythema RLE, some erythema LLE. D/c IV atbs, take augmentin and doxycycline PO x 7 days.

    49. Overview of Physician Consults • Overview: • GI consult for HE → rifaximin, lactulose to improve mentation • Nephrology consult for worsening acute renal failure (Cr 3.4 to 3.8)  dialysis, d/c IVF, water flush 250 ml q6h via NGT, lasix. • Assessment: No improvement with IV fluid. Hypernatremia – related to NPO status. Hypokalemia – related to lactulose and multiple BMs. Ascites • Infectious Disease Consult for Cellulitis → augmentin and doxycycline • NUTRITION: At this point, nutrition has not been discussed, pt has consumed some jello but that is all.

    50. Overview of Lab Values