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1Suzanna Ndraha, 2Marcellus Simadibrata 1 Department of Internal Medicine, Faculty of Medicine, University of Indonesia 2 Division of Gestroenterology, Department of Internal Medicine, Faculty of Medicine, University of Indonesia
Abstrak Introduksi: Asupan protein berlebih dapat menyebabkan ensefalopati hepatikum (EH). Pembatasan protein menjadi kontroversi karena memperburuk malnutrisi. Artikel ini melaporkan kasus EH gizi kurang yang mendapat terapi L-ornitin-L-aspartat (LOLA) disertai diet protein adekuat sesuai dengan status nutrisinya. Kasus: Pasien laki-laki 62 tahun datang dengan keluhan utama penurunan kesadaran sejak 6 jam sebelumnya. Dia telah diketahui menderita penyakit sirosis sejak 6 tahun. Beberapa hari sebelumnya pasien makan banyak putih telur dan ikan. Pada pemeriksaan fisik didapatkan gizi kurang dan kesadaran delir. Encefalopati hepatikum ditegakkan berdasarkan hasil critical flicker test (CFF) yang rendah, dan kadar amonia darah yang tinggi. Pasien mendapatkan diet 35 kcal/kg per hari dan protein 1.5 g/kg/hari. LOLA diberikan untuk menurunkan ammonia darah dan meningkatkan angka critical flicker test. Dalam pemantauan selajutnya didapatkan pasien membaik, critical flicker test (CFF) meningkat dan ammonia darah menurun. Diskusi: Pada kasus ini, EH diterapi dengan LOLA tanpa retriksi protein. EH yang membaik, dalam hal ini kemungkinan akibat LOLA membantu menurunkan kadar amonia darah. Kesimpulan Dengan memberikan LOLA yang dapat menurunkan kadar amonia darah, EH dengan malnutrisi dapat diterapi dengan nutrisi adekuat. Kata-kata kunci: sirosis hati, ensefalopati, L-ornitin L-aspartat, critical flicker test, kadar ammonia darah Abstract Introduction: Excessive protein intake can cause hepatic encephalopathy (HE). Constricting protein in HE is becoming a controversy, because it can worsen malnutrition. This article reports the case of an under nutrition HE which is treated with L-ornithine-L-aspartate (LOLA) and given appropriate diet according to the nutrition status Case A 62-year-old man came with chief complaint of reduced consciousness since 6 hours before admission. He had been diagnosed as liver cirrhosis for 6 years. Several days prior to admission he took high protein diet. Physical examination revealed under nutrition and unconsciousness. Hepatic encephalopathy was confirmed with low critical flicker test (CFF), and high blood ammonia level. He was treated with adequate diet and LOLA to decrease blood ammonia and improve the CFF. During the treatment, consciousness improved to normal, CFF increased and ammonia level decreased.
7]. where most of it considered as minimal HE. With the intake of LOLA intend to reduce the ammonia level in the blood. besides to overcome the initiating factor. The efforts to reduce the amount of ammonia in the blood are done by giving lactulose.Discussion In this case of HE was treated with LOLA without protein restriction. From his present history of illness. because it can worsen malnutrition . Due to that. so that it is unnecessary to constrict protein intake in liver cirrhosis patient with malnutrition. blood ammonia level Introduction Liver cirrhosis is the end of various type of liver disease.5]. and portal hypertension with all its complications [1.10]. LOLA nowadays started to be used to overcome EH cause its proven can reduce ammonia level in the blood . Constricting protein intake in HE nowadays is becoming a controversy. Case Patient is a 62 years old man who was brought in the emergency ward with chief complaint of reduced consciousness which manifested as having difficulty in speaking since 6 hours prior to hospital admission. Key words: liver cirrhosis. reduce liver capability for detoxification (Hepatic Encephalopathy). which is needed for ammonia detoxification. For the nutrition improvement a diet 25-35 kcal/Kg per day and protein 1-1. LOLA stimulates the urea cycle and glutamine synthesis. patient constantly feels drowsy therefore his sleeping hours have increased in both duration and . it can evoke various complications such as reduce of liver synthetic function (coagulopathy). Contrariwise nutrition improvement can increase muscle mass. critical flicker test. Conclusion: By giving LOLA to decrease blood ammonia level. HE with malnutrition could be treated with adequate nutrition. Furthermore. hepatic encephalopathy. among others is the effect of over intake protein and gastrointestinal bleeding. This article reports the case of hepatic encephalopathy which is treated with LOLA and given 35 kcal/kg/day diet and 1. patient has been experiencing fatigue and loss of balance since 3 days prior to admission. Few research reports that malnutrition can increase mortality rate in liver cirrhosis [6. in this circumstance maybe cause of LOLA treatment that helps decreasing the plasma ammonia level. The EH improved.5g/kg/day protein. L-ornithine L-aspartate. the management of HE especially tend to reduce the amount of ammonia in the blood. Hepatic Encephalopathy (HE) is one of all liver cirrhosis that brings high morbidity and mortality effect.5g/Kg/day is suggested. . and constrict the protein intake. until now is considered to have the major role in HE pathogenesis [4. Increases of ammonia level in the blood. The incidence rate of HE in liver cirrhosis are various from 30-45%  and also 50-70% . which is the important mechanism in ammonia detoxification [9.2]. antibiotics for intestine sterilization.
patient’s serum albumin level had been low. Ammonia level shows 189 mol/L (normal < 50 mol/L). His symptoms were swollen abdomen and feet which resolved every time he received medications from the doctor. normal prothrombine time. no signs of fever. Patient was diagnosed with liver cirrhosis due to hepatitis B infection 6 years prior to admission. After 2 days of treatment. Pancytopenia was suspected due to hypersplenism with liver cirrhosis. further deterioration of speech skills therefore family members decided to bring him to the emergency ward of RS Tebet Jakarta. since several days prior to admission. SGPT 32 iu/L.7 g/dl.4 g/dl albumin level. In addition. USG of the abdomen is planned to confirm the cirrhosis. collateral veins were discovered on his abdomen with enlarged spleen up to shuffner II. L-ornithine L-aspartate (Hepamerz) I. LED 50 mm/jam. During physical examination in the emergency ward.98 mg/dl. Other abnormalities seen were spider nevi on the chest and palmar erythem on his extremities.frequency and family members are often unable to comprehend what the patient says. Lactulose of PO 4 x 15 ml is administered to facilitate transit to reduce further breakdown of ammonia. Current working diagnosis on arrival is hepatic encephalopathy due to increased protein intake on cirrhotic patient due to chronic hepatitis B infection. During the follow up. Encephalopathy diagnosis was proven with the increased of ammonia level. we acquired the abdominal USG results which confirmed the diagnosis of liver cirrhosis and splenomegaly with minimal ascites. These results further strengthen the diagnosis of hepatic encephalopathy on liver cirrhosis. with no signs of ascites or extremity edema. To confirm this diagnosis. however abnormalities were found in his eyes which had anemic conjunctiva and icteric sclera. patient was deemed with severely ill condition. CFF has increased up to 38. Repeated measurement of blood ammonia levels shows an improvement (reduction up to155mol/L) and furthermore. he was unable to recognize the people around him.8 Hz. furthermore. leukocyte 3270/uL.98 mg/dl total bilirubin level.600/uL. blood ammonia level as well as critical flicker test (CFF) to confirm hepatic encephalopathy. and a flapping tremor was also noticeable. His body height was 168 cm. and no flapping tremor was noticeable. Albumin 2.8 Hz (normal ≥ 39 Hz). patients condition improved with increased consciousness level up to fully alert. 1. delirious. CFF 33. SGOT 75 iu/L. However. minimal ascites (under control) and minimal encephalopathy . 20 grams of (4 ampoules) /day in 250 ml of infuse line for 5 days and later replaced with oral route 3 x 6 grams for 2 weeks in order to reduce the ammonia levels in the blood. therefore his wife decided to add more fish into his daily diet. He always performed his check-up routinely every month up to this incident. total bilirubin 1. Laboratory results shown 2. he also pays high attention on his daily diet which was specifically recommended by a nutritionist. Urinalysis tests showed no abnormalities and were under normal limits. Patient is given a diet of 2100 calories daily with 90 grams protein along with substituted branch chained amino acids (BCAA). Discussion This is a case of liver cirrhosis with the complication of encephalopathy due to excessive protein intake. Excessive protein intake is one of several initiating factor of HE that cause increased ammonia production . Electrolyte balance and prothrombine time were under normal limits. his weight was at 62 kg and mid arm muscle circumference (MAMC) of 228 mm. Laboratory results on admission showed a condition of pancytopenia (Hb 11. He had normal blood pressure.4 g/dl. supported the theory that acknowledge that ammonia hold an important role in the HE mechanism. platelets 65.V. 6 hours prior to admission.
EH is improving due to LOLA treatment which can reduce plasma ammonia level. 25 (Suppl.1 kg/m2 BMI (Body Mass Index) that shows normal nutritious. The patient is given appropriate diet according to the nutrition status to avoid worsening of the malnutrition. patient is given LOLA 20 g intravenous (4 ampoules dissolved in 250 cc carrier solution over 4 hours) for 5 days followed by LOLA granules 6 g three times daily for 2 weeks. but apparently from MAMC shows that actually the patient has started to undergo minor malnutrition. It appears that the diet treatment given to this patient did not worsen EH. Review article: the burden of hepatic encephalopathy. simple. Schliess F. The patient has 22. El-Serag H. therefore calculation and measurement using MAMC is more suggested to evaluate nutrition status . Jayakumar AR. The peripheral benzodiazepine receptor and neurosteroids in the pathogenesis of hepatic encephalopathy and amonia neurotoxicity. 1): 3–9 5. Buku Ajar Ilmu Penyakit Hati. Burden of Liver Disease in the United States: Summary of Workshop. et al. Rama Rao KV. Kramer L. Journal of Gastroenterology and Hepatology 2002. The CFF of 33. Gendo A. Management of Hepatic Encephalopathy. Brown RS. Nutritional support in patients with chronic liver disease. 2002. It was known that the weight of liver cirrhosis patients is more affected by ascites and edema. nutritional status in liver cirrhosis was measured base on MAMC. Hepatology 2000. Saudi J Gastroenterol 2006.335-45 3. Nature clinical practice. Kusumobroto HO. in order to maintain the nutrition status. Poordad FF.12:8-15 8. Kircheis G. Kim WR.31:30-34. 92:795–812 2. Patient is treated with adequate nutrition. in this circumstance maybe cause of LOLA treatment that helps decreasing the plasma ammonia level. Jakarta: Jayabadi. and reliable to diagnose minimal HE in liver cirrhosis [11.36(1):227-42 4. Panickar KS. EH was diagnosed based on CFF and blood ammonia level. Norenberg MD. 1st ed. 2006. Noer HMS. References 1.8 0. An evidence-based update on hepatic encephalopathy. p.17:S260-7 . In Häussinger. Häussinger D. Henkel AS. Tribl B. 2006.shown that liver function level of the patient is classified as Child Pugh B so the possibility of HE due to endogen factor is not likely.58 Hz in this patient showed the existence of HE cause by increased ammonia level due to increased protein intake priory. To overcome the risk of increasing ammonia level. 12]. Munoz SJ. with branch chain amino acid (BCAA) substitute. Conclusion In this case. Hepatic Encephalopathy. However. Flicker test nowadays considered as a sensitive test. Terrault NA. Dalam Sulaiman HA. The Netherlands: Springer. Hepatology. Hepatic Encephalopathy and nitrogen metabolism. 6. Ference P. Aliment Pharmacol Ther. Buchman AL. Gastroenterology and Hepatology 2006. Conference Proceedings. Sirosis hati.3(4): 202-09 9. p. Kircheis G. Lesmana LA. Zauner C. 2007. 143-59 7. Abdo AA. Partial Pressure of Ammonia Versus Ammonia in Hepatic Encephalopathy. 2008. Akbar HN. Schneider B. Med Clin N Am.
Wettstein M. Bengtsson M. Olsson R. Malnutrition and diabetes mellitus are related to hepatic encephalopathy in patients with liver cirrhosis. Record C O. Timmermann L. Critical flicker frequency: It is time to break down barriers surrounding minimal hepatic encephalopathy. Gut 2000. placebo controlled trial.47:10–11 13. Kalaitzakis E.47:571–574 11.10. Rees C J. Hepatology 2002.27(9):1194-201 . Liver International 2007. Gomez MR. Hudson M. Kircheis G. et al. Schitzler A. Al Mardini H. Oppong K. Critical Flicker Frequency for quantification of low grade hepatic encephalopathy.35:35766 12. Effect of L-ornithine-L aspartate on patients with and without TIPS undergoing glutamine challenge: a double blind. Journal of Hepatology 2007. Häussinger D. Hugosson I. Henfridsson P. Jalan R.
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