Thursday, November 24, 2016

Ringkasan: Bimbingan Penelitian IPD-15


Ringkasan: Bimbingan Penelitian IPD-15

disampaikan oleh dr Suzanna Ndraha SpPD KGEH FINASIM

diringkas oleh: Edison Wiryo



Pada pelaksanaan penelitian kita perlu membuat proposal penelitian terlebih dahulu, yang terdiri dari: 
  • Abstrak berisi rangkuman penelitian yang dilakukan. Abstrak yang baik berisi tidak lebih dari 250 kata. Di bawah abstrak kita harus mencantumkan kata kunci (keywords), yakni kata penting yang menjadi topik paling penting dari seluruh penelitian yang telah dilakukan. Kata kunci yang baik terdiri dari 3 hingga 5 kata kunci.
  • Bab I: Pendahuluan. Bagian pendahuluan bertujuan meyakinkan pembaca bahwa penelitian yang dilakukan layak dan penting untuk diketahui oleh kalangan yang dituju. Latar belakang yang dipilih juga harus jelas tujuan dan manfaat penelitian, serta rumusan masalah mengapa dilakukan penelitian. Pertanyaan -pertanyaan yang dijadikan rumusan masalah harus dapat terjawab untuk memberikan kesimpulan pada akhir penelitian. Tujuan dan manfaat penelitian tidak boleh terlepas dari rumusan masalah dan pertanyaan penelitian. Hipotesis harus berdasarkan jawaban sementara atas pertanyaan penelitian.
  • Bab II: Tinjauan pustaka, kerangka teori dan kerangka konsep. Tinjauan pustaka yang dibuat harus bersumber dari literatur-literatur resmi dan terpercaya yang dipublikasikan maksimal 10 tahun sebelum penelitian dilakukan. Harus diperhatikan pula penggunaan superscript untuk menunjang kepustakaan. Kerangka teori adalah diagram dari tinjauan pustaka yang didalamnya terdapat kerangka konsep. Kerangka konsep sendiri itu adalah diagram yang menunjukkan jenis serta hubungan antar variabel yang diteliti.
  • Bab III: Metode penelitian. pada metoda penelitian berisikan data-data dan cara pengambilan data seperti desain, tempat dan waktu pengambilan sampel, populasi sampel, cara pengambilan sampel, besar sampel, kriteria inklusi dan eksklusi, identifikasi variabel, batasan operasional, alur penelitian, cara kerja yang detil, analisis datam masalah etika, jadwal penelitian, anggaran penelitian. 
  • Bab IV: Hasil penelitian. Hasil penelitian merupakan data-data yang didapatkan selama penelitian, baik data kategorik maupun numerik. Data dapat disajikan dalam bentuk tabel, diagram, gambar, dan lain-lain.
  • Bab V: PembahasanPada pembahasan, kita membandingkan hasil penelitian yang dilakukan dengan penelitian lain. Pembahasan harus dalam sehingga setiap pernyataan yang diungkapkan dalam penelitian memiliki dasar yang kuat. Kesimpulan dicantumkan sebagai penutup hasil penelitian. Hal penting di sini adalah, kesimpulan harus dapat menjawab pertanyaan dalam rumusan masalah di bab pendahuluan.
  • Daftar pustaka. merupakan daftar dari literatur-literatur resmi yang dipakai sebagai pedoman pada bagian pembahasan dan sebaiknya ditulis dalam format international seperti Vancouver.

Wednesday, November 23, 2016

IPD 15 : Ringkasan Bimbingan Cairan

RINGKASAN BIMBINGAN IPD- 13: TERAPI CAIRAN


Disampaikan oleh: Dr Suzanna Ndraha SpPD KGEH




Diringkas oleh: Rionaldo Sanjaya

Terapi cairan sangat diperlukan dalam mengganti kebutuhan cairan yang hilang. Seringkali pasien yang dirawat dilakukan pemasangan infus, apa saja indikasi pemasangan infus ? 

A. Indikasi Pemasangan Infus
               1. Syok hipovolemik


Syok hipovolemik bisa disebabkan karena adanya perdarahan atau diare, dan ditandai dengan adanya akral dingin, takikardi, dan hipotensi. Pada syok hipovolemik biasanya diberikan cairan kristaloid (Nacl, RL, Asering) atau cairan koloid. Jika syok disebabkan karena perdarahan (>20%), maka syok dapat ditangani dengan pemberian infus NaCl terlebih dahulu sebelum dilakukan pemberian tranfusi.

2.  Pemberian obat secara drip / Koreksi
Pemberian obat secara drip seperti insulin, fenitoin, tramadol, dopamin, dsb. Pelarut dalam pemberian obat drip bisa dengan NaCl atau Dekstrose 5%.
Koreksi gangguan elektrolit ataupun asam basa juga memerlukan pemasangan infus. Jika sudah terjadi asidosis metabolik berat memerlukan koreksi bikarbonat. Keperluan bikarbonat dihitung dengan rumus = 0.3 x BE x BB. Pada koreksi bikarbonat pelarut yang baik yaitu Dekstrose 5%, karena pada penggunaan NaCl dapat terjadi garam dan mengendap sehingga kurang efektif. Pada Kasus Ketoasidosis diabetikum mulai dikoreksi bila pH darah < 7.1.
Koreksi Kalium pada hipokalemia berat / kadar kalium <2.5mmol/L sangat diperlukan karena mudah terjadi gangguan irama jantung. Koreksi kalium dengan KCl dihitung dengan rumus ( 0.3 x ∆K x BB ) + Maintenance, Koreksi kalium baik dalam pelarut non dekstrose karena dekstrose akan merangsang pengeluaran insulin dan pengeluaran insulin akan menarik Kalium ke intrasel sehingga kurang efektif kecuali pada kasus hipoglikemia.
Koreksi Natrium diberikan pada pasien dengan kadar natrium <125mmol/L, dikoreksi dengan NaCl 3% diberikan tidak boleh lebih dari 6tpm karena dapat menimbulkan gangguan pada batang otak.
3.  Transfusi
Sebelum dilakukan tranfusi, biasanya diberikan larutan NaCl fisiologik terlebih dahulu sebagai persiapan tranfusiKomponen darah terdiri dari sel darah merah, sel darah putih, trombosit dan plasma. Sel darah putih jarang ditransfusi karena bersifat sangat imunogenik .
  •           Sel darah merah
a.       Whole blood : Perdarahan akut
b.      Washed PRC: Incompatible major (AIHA) / inkompatibilitas minor gr 3/4
c.       PRC biasa: Anemia kronik
d.      Leukocyte depleted : Reaksi imunologi
  •        Trombosit
  •           Trombocyte cocentrate
·                                          Indikasi transfusi trombosit adalah:
-                              Gagal sumsum tulang
                        a.       Target Tr > 20,000 tanpa resiko perdarahan
                        b.      Target Tr > 50,000 dengan resiko perdarahan
              Reaksi imunologi misalnya penyakit ITP dan DBD bukan merupakan indikasi transfusi trombosit. Tapi,     pada DBD trombosit diberikan kalau terjadi perdarahan masif (hematemesis melena) dengan Tr < 100,000. 1 unit TC dapat menaikkan trombosit sebanyak 10,000. 
  •           Plasma
                       a.       FFP: diberikan pada pasien defisiensi faktor koagulasi
                       b.      Plasma biasa: 
                          - tidak ada faktor koagulasi
                          - mengandungi albumin
                          - berfungsi sebagai koloid tapi jarang diberikan karena sudah ada koloid sintetik.


    4. Nutrisi
         Terutama pada pasien yang dipuasakan seperti pada kasus akan dilakukan suatu tindakan ( seperti pada Colonoskopy, Operasi, BNO IVP ) , ileus , pankreatitis, dan sebagainya sehingga memerlukan IUFD nutrisi.     

  Nutrisi ini perlu diberikan untuk memenuhi kebutuhan manusia yaitu:
            a)      Kalori basal         :
Laki-laki:               30 kkal/kgBB
Wanita  :               25 kkal/kgBB
Dalam 3 hari pertama, kita boleh memberikan kalori di bawah kebutuhan. Pada hari pertama diinfus, kalori dapat diberikan ¼ dari kebutuhan total, Pada hari kedua, dapat diberikan ½ dari kebutuhan total dan hari ketiga dapat diberikan 75% dari kebutuhan total kalori. Tetapi, pada hari keempat, seluruh kebutuhan kalori total harus diberikan pada pasien.

             b)      Protein                 : 0,8 g/ kgBB
Pada hari pertama pemberian protein dapat ditunda dulu kecuali kalau pasien tersebut malnutrisi atau mengalami hypoalbuminemia. Tetapi pada hari keempat, pemberian harus sesuai kebutuhan total protein.
Untuk memenuhi kebutuhan protein pada pasien yang hypoalbuminemia, harus diberikan cairan protein berkonsentrasi tinggi misalnya Triofusin (1000 cc = 1000 kalori). Pemberian protein konsentrasi tinggi ini mempunyai osmolaritas tinggi sehingga pemberiannya tidak boleh melalui vena perifer tetapi harus melalui vena sentral yaitu dengan pemasangan CVP. Batas osmolaritas cairan yang dapat masuk ke vena perifer adalah < 900 osm.

           c)       Elektrolit
a.       Natrium               : 1-2 mEq/ kgBB
b.      Kalium                  : 1 mEq/ kgBB

           d)      Cairan                   : 30-50 cc/ kgBB
Elektrolit dan cairan harus diberikan sesuai kebutuhan total sejak dari hari pertama pemberian.

Contoh Kasus :  Seorang pasien akan diberikan IUFD clinimix 1000 dan aminofluid 1000 berapa kadar elektrolit, kalori, dan protein yang masuk?             
                                    Na             K              Cal            Protein
 Aminofluid 1000        35meq      20meq        420kkal          30g
 Clinimix 1000            70meq      60meq        510kkal           -

5. Emergency Line
Seperti pada kasus Decompensatio cordis, Aritmia, stroke hemoragik

Wednesday, November 2, 2016

CONTOH CASE REPORT


CONTOH CASE REPORT

L-ornithin L-aspartate in Hepatic Encephalopathy due to Liver Cirrhosis
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
Pasien laki-laki 62 tahun dibawa ke ruang gawat darurat RS Tebet Jakarta dengan keluhan utama penurunan kesadaran sejak 6 jam sebelumnya.  Dia telah diketahui menderita penyakit liver sirosis sejak 6 tahun, akibat hepatitis B. Beberapa hari sebelumnya pasien makan banyak putih telur dan ikan karena tahu albumin darahnya rendah Pada pemeriksaan fisik didapatkan keadaan gizi kurang, kesadaran delir, ada flapping tremor. Encefalopati hepatikum ditegakkan berdasarkan hasil critical flicker test (CFF) yang rendah (33,8 ± 0,58 Hz), dan kadar amonia darah yang tinggi (189 mmol/L). Pasien mendapatkan diet 35 kcal/kg per hari dan  protein 1.5 g/kg/ha ri. L-ornithine L-aspartate diberikan untuk menurunkan ammonia darah dan meningkatkan angka critical flicker test. Dalam pemantauan selajutnya didapatkan pasien membaik, kesadaran berangsur normal, critical flicker test (CFF) meningkat dan ammonia darah menurun.
Key words: sirosis hati, ensefalopati, L-ornitin L-aspartat, critical flicker test, kadar ammonia darah

Abstract
A 62-year-old man was brought into emergency room of Tebet Hospital Jakarta, Indonesia, with chief complaint of reduced consciousness since 6 hours before admission. He had been diagnosed as liver cirrhosis for 6 years, due to chronic hepatitis B infection. Several days prior to admission he took high protein diet, in order to reach normal blood albumin level. Physical examination revealed unconsciousness and flapping tremor. Hepatic encephalopathy was confirmed with critical flicker test (CFF) less than normal (33,8 ± 0,58 Hz), and blood ammonia level higher than normal (189 mmol/L). He was treated with diet 35 kcal/kg per day and  protein 1.5 g/kg/day, L-ornithine L-aspartate to decrease blood ammonia and improve the critical flicker test. During the treatment, the patient’s condition improved, level of consciousness improved to normal, critical flicker test (CFF) increased and blood ammonia level decreased.
Key words: liver cirrhosis, hepatic encephalopathy, L-ornithine L-aspartate, critical flicker test, blood ammonia level

Introduction
. Liver cirrhosis is the end of various type of liver disease, it can evoke various complications such as reduce of liver synthetic function (coagulopathy), reduce liver capability for detoxification (Hepatic Encephalopathy), and portal hypertension with all its complications [1,2]. Hepatic Encephalopathy (HE) is one of all liver cirrhosis that brings high morbidity and mortality effect. The incidence rate of HE in liver cirrhosis are various from 30-45% [3] and also 50-70% [4], where most of it considered as minimal HE.
Increases of ammonia level in the blood, among others is the effect of over intake protein and gastrointestinal bleeding, until now is considered to have the major role in HE pathogenesis [4,5]. Due to that, the management of HE especially tend to reduce the amount of ammonia 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, antibiotics for intestine sterilization, and constrict the protein intake. Constricting protein intake in HE nowadays is becoming a controversy, cause it can worsen malnutrition [6]. Few research reports that malnutrition can increase mortality rate in liver cirrhosis [6,7]. Contrariwise nutrition improvement can increase muscle mass, which is needed for ammonia detoxification. For the nutrition improvement a diet 25-35 kcal/Kg per day and protein 1-1.5g/Kg/day is suggested. 
L-ornithine-L-aspartate (LOLA) nowadays started to be used to overcome EH cause its proven can reduce ammonia level in the blood [8], LOLA stimulates the urea cycle and glutamine synthesis, which is the important mechanism in ammonia detoxification [9,10]. With the intake of LOLA intend to reduce the ammonia level in the blood, so that it is unnecessary to constrict protein intake in liver cirrhosis patient with malnutrition.
This article reports the case of hepatic encephalopathy which is treated with L-ornithine-L-aspartate (LOLA) and given 35 kcal/kg/day diet and 1.5g/kg/day protein.
.
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. From his present history of illness, patient has been experiencing fatigue and loss of balance since 3 days prior to admission. Furthermore, patient constantly feels drowsy therefore his sleeping hours have increased in both duration and frequency and family members are often unable to comprehend what the patient says. 6 hours prior to admission, he was unable to recognize the people around him, further deterioration of speech skills therefore family members decided to bring him to the emergency ward of RS Tebet Jakarta.
Patient was diagnosed with liver cirrhosis due to hepatitis B infection 6 years prior to admission. His symptoms were swollen abdomen and feet which resolved every time he received medications from the doctor. He always performed his check-up routinely every month up to this incident; furthermore, he also pays high attention on his daily diet which was specifically recommended by a nutritionist. However, since several days prior to admission, patient’s serum albumin level had been low, therefore his wife decided to add more fish into his daily diet.
During physical examination in the emergency ward, patient was deemed with severely ill condition, delirious. His body height was 168 cm; his weight was at 62 kg and mid arm muscle circumference (MAMC) of 228 mm. He had normal blood pressure, no signs of fever, however abnormalities were found in his eyes which had anemic conjunctiva and icteric sclera. Other abnormalities seen were spider nevi on the chest and palmar erythem on his extremities. In addition, collateral veins were discovered on his abdomen with enlarged spleen up to shuffner II, with no signs of ascites or extremity edema, and a flapping tremor was also noticeable.
Laboratory results on admission showed a condition of pancytopenia (Hb 11,7 g/dl, leukocyte 3270/uL, platelets 65.600/uL, LED 50 mm/jam. Electrolyte balance and prothrombine time were under normal limits. Albumin 2,4 g/dl, total bilirubin 1,98 mg/dl, SGOT 75 iu/L, SGPT 32 iu/L. Urinalysis tests showed no abnormalities and were under normal limits.
            Current working diagnosis on arrival is hepatic encephalopathy due to increased protein intake on cirrhotic patient due to chronic hepatitis B infection. Pancytopenia was suspected due to hypersplenism with liver cirrhosis. To confirm this diagnosis, USG of the abdomen is planned to confirm the cirrhosis, blood ammonia level as well as critical flicker test (CFF) to confirm hepatic encephalopathy.  Patient is given a diet of 2100 calories daily with 90 grams protein along with substituted multiple chained amino acids (AARC),  L-ornithine L-aspartate (HepamerzÒ) I.V.  20 grams of (4 ampoules) /day in 250 ml of infuse line for 5 days and later replaced with oral route dose of 3 x 6 gram for 2 weeks in order to reduce the ammonia levels in the blood. Lactulose of PO 4 x 15 ml is administered to facilitate transit to reduce further breakdown of ammonia.
            During the follow up, we acquired the abdominal USG results which confirmed the diagnosis of liver cirrhosis and splenomegaly with minimal ascites. Ammonia level shows 189 mmol/L (normal < 50 mmol/L), CFF 33,8 ± 0,58 Hz (normal ≥ 39 Hz). These results further strengthen the diagnosis of hepatic encephalopathy on liver cirrhosis. After 2 days of treatment, patients condition improved with increased consciousness level up to fully alert (compos mentis), and no flapping tremor was noticeable. Repeated measurement of blood ammonia levels shows an improvement (reduction up to155mmol/L) and furthermore, CFF has increased up to 38.8 ± 0.62 Hz.

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 [11]. Encephalopathy diagnosis was proven with the increased of ammonia level, supported the theory that acknowledge that ammonia hold an important role in the HE mechanism. Laboratory results shown 2,4 g/dl albumin level, 1,98 mg/dl total bilirubin level, normal prothrombine time, minimal ascites (under control) and minimal encephalopathy 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.
Flicker test nowadays considered as a sensitive test, simple, and reliable to diagnose minimal HE in liver cirrhosis [12, 13]. The Critical Flicker Test (CFF) of 33,8 ± 0,58 Hz in this patient showed the existence of HE cause by increased ammonia level due to increased protein intake priory. 
The patient has 22, 7 kg/m2 BMI (Body Mass Index) that shows normal nutritious, but apparently from MAMC shows that actually the patient has started to undergo minor malnutrition. It was known that the weight of liver cirrhosis patients is more affected by ascites and edema, therefore calculation and measurement using MAMC is more suggested to evaluate nutrition status [14]. Patient is treated with 2100 calories diet, 90 gram of protein with branch chain amino acid (BCAA) substitute, in order to maintain the nutrition status. To overcome the risk of increasing ammonia level, patient is given L-ornithine-L-aspartate (LOLA) 20 g intravenous (4 ampoules dissolved in 250 cc carrier solution over 4 hours) for 5 days followed by L-ornithine-L-aspartate granules 6 g three times daily for 2 weeks. It appears that the diet treatment given to this patient did not worsen EH, in this circumstance maybe cause of LOLA treatment that helps decreasing the plasma ammonia level.

Conclusion
This case reports liver cirrhosis that nutrition status was measured base on MAAC, EH was diagnosed based on CFF (critical flicker test), then for this case, patient is given appropriate diet according to the nutrition status to avoid worsening of the malnutrition. However, EH is improving due to LOLA treatment which can reduce plasma ammonia level.

References
1.     Munoz SJ. Hepatic Encephalopathy. Med Clin N Am. 2008; 92:795–812
2.     Kusumobroto HO. Sirosis hati. Dalam Sulaiman HA, Akbar HN, Lesmana LA, Noer HMS. Buku Ajar Ilmu Penyakit Hati. 1st ed. Jakarta: Jayabadi; 2007. p.335-45
3.     Kim WR, Brown RS, Terrault NA, El-Serag H. Burden of Liver Disease in the United States: Summary of Workshop. Hepatology. 2002;36(1):227-42
4.     Poordad FF. Review article: the burden of hepatic encephalopathy. Aliment Pharmacol Ther. 2006; 25 (Suppl. 1): 3–9
5.     Kramer L, Tribl B, Gendo A, Zauner C, Schneider B, Ference P. et al. Partial Pressure of Ammonia Versus Ammonia in Hepatic Encephalopathy. Hepatology 2000;31:30-34.
6.     Norenberg MD, Jayakumar AR, Rama Rao KV, Panickar KS. The peripheral benzodiazepine receptor and neurosteroids in the pathogenesis of hepatic encephalopathy and amonia neurotoxicity. In Häussinger, Kircheis G, Schliess F. Hepatic Encephalopathy and nitrogen metabolism. The Netherlands: Springer; 2006. p. 143-59
7.     Abdo AA. An evidence-based update on hepatic encephalopathy. Saudi J Gastroenterol 2006;12:8-15
8.     Anne S Henkel and Alan L Buchman. Nutritional support in patients with chronic liver disease. Nature clinical practice. Gastroenterology and hepatology. 2006;3(4): 202-09
9.     Kircheis G, Häussinger D. Management of Hepatic Encephalopathy. Conference Proceedings. Journal of Gastroenterology and Hepatology 2002;17:S260-7 
10.  Rees C J, Oppong K, Al Mardini H, Hudson M, Record C O. Effect of L-ornithine-L aspartate on patients with and without TIPS undergoing glutamine challenge: a double blind, placebo controlled trial.  Gut 2000;47:571–574
11.  Santiago J. Munoz, MD. Hepatic Encephalopathy.  Med Clin N Am 2008; 92:795–812.
12.  Kircheis G, Wettstein M, Timmermann L, Schitzler A, Häussinger D. Critical Flicker Frequency for quantification of low grade hepatic encephalopathy. Hepatology 2002;35:357-66 
13.  Gomez MR. Critical flicker frequency: It is time to break down barriers surrounding minimal hepatic encephalopathy. Journal of Hepatology  2007;47:10–11
14.  Kalaitzakis E, Olsson R, Henfridsson P, Hugosson I, Bengtsson M, Jalan R. et al. Malnutrition and diabetes mellitus are related to hepatic encephalopathy in patients with liver cirrhosis. Liver International 2007;27(9):1194-201



Case report ini dipublikasi di majalah ACTA MEDICA Vol 42 • No 3 • Juli 2010 hal 158-161