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"Latar belakang: Morbiditas akibat duktus arteriosus paten (DAP) pada neonatus cukup bulan (NCB) cukup tinggi. Peran prostaglandin E2 (PGE2), trombosit (immature platelet fraction, IPF), dan vascular endothelial growth factor (VEGF) pada penutupan DA secara fungsional dan anatomis pada NCB belum banyak diteliti. Patofisiologi terjadinya DAP dapat memengaruhi tata laksana farmakologi dini yang belum terstandardisasi pada NCB. Penggunaan obat antiinflamasi nonsteroid seperti ibuprofen dimungkinkan dapat menghambat jalur sintesis prostaglandin dengan efek samping minimal.Tujuan: Mengkaji peran prostaglandin E2, VEGF, IPF, dan efek pemberian ibuprofen oral dalam proses penutupan DA pada NCB.Metode: Penelitian dilakukan di rumah sakit (RS) Sanglah Denpasar, RS Prima Medika Denpasar, dan RS Umum Daerah Wangaya Denpasar, dalam periode Maret sampai Agustus 2015. Penelitian terdiri dari 2 desain, pertama desain potong lintang pada pasien dengan DAP dan tanpa DAP secara consecutive sampling dan desain kedua uji klinis acak terkontrol ganda pada pasien DAP usia ≥ 48 jam. Pasien dengan DAP kemudian dimasukkan dalam uji klinis, dilakukan randomisasi untuk diberikan perlakuan ibuprofen oral dosis hari pertama 10 mg/kg, hari kedua dan ketiga 5 mg/kg atau plasebo. Pemantauan hemodinamik dan efek samping obat dilakukan selama pemberian perlakuan. Pemeriksaan ekokardiografi, PGE2, VEGF, IPF, dan kreatinin dilakukan pada hari pertama dan keempat pascapemberian perlakuan.Hasil: Terdapat 64 subjek yang diteliti pada desain pertama dan 32 subjek pada desain kedua. Rerata kadar PGE2 lebih tinggi pada kelompok dengan DAP dibanding tanpa DAP, sedangkan rerata kadar VEGF dan IPF tidak berbeda. Ibuprofen oral tidak terbukti menurunkan diameter DA pascaperlakuan, tidak terdapat perbedaan rerata diameter pada kedua kelompok. Terdapat hubungan positif sedang terhadap perubahan kadar PGE2 dengan perubahan diameter DAP pascaperlakuan. Tidak terdapat perubahan hemodinamik atau efek samping akibat pemberian ibuprofen oral atau plasebo pada NCB dengan DAP.Simpulan: Tingginya kadar PGE2 terbukti berperan dalam patensi DA pada NCB. Ibuprofen oral dosis 10 - 5 - 5 mg/kgBB tidak mengecilkan diameter DAP.

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Background: Serious morbidity impact due to patent ductus arteriosus (PDA) in full-term neonates remains high. The functional role of prostaglandin E2 (PGE2), platelet (immature platelet fraction, IPF), and vascular endothelial growth factor (VEGF) has not been studied in the closure mechanism of ductus arteriosus (DA). Understanding of pathophysiology of PDA may influence early pharmacological treatments, which have not been standardized in full-term neonates. The use of non-steroidal anti-inflammatory drugs such as ibuprofen can be beneficial as a pharmacological agent in enhancing the closure of PDA with minimal adverse effects.

Objectives: To evaluate the role of prostaglandin E2, VEGF, IPF, and the effect of oral ibuprofen in the process of DA closure in full-term neonates.

Methods: This study was conducted in Sanglah General Hospital, Prima Medika Hospital, and Wangaya Hospital Denpasar. The study consisted of two designs, the first was cross-sectional design in subjects with and without PDA using consecutive sampling and the second was double blind randomized controlled trial in full-term infant aged ≥ 48 hours. Subjects with PDA were randomized to oral ibuprofen and placebo administration, in which ibuprofen was given consecutively 10 - 5 - 5 mg/kg. All subjects underwent echocardiography, PGE2, VEGF, and IPF assays. Hemodynamics monitoring was evaluated during trial and adverse effect due to ibuprofen was recorded by measuring urine volume and plasma creatinine level.

Results: From March to August 2015, there were 64 subjects recruited for the first design and 32 subjects in the second design. The mean level of PGE2 was higher significantly in the group with PDA than non PDA group, while the mean levels of VEGF and IPF showed no difference. In the second design, oral ibuprofen showed no effect in reducing DA diameter after treatment. There were no differences in mean diameter of DA in both groups before and after treatments. There was moderate positive relationship between levels of PGE2 and the change of PDA diameter. There were neither hemodynamic changes nor adverse effect due to the administration of oral ibuprofen or placebo.

Conclusions: A high level of PGE2 appears to play a pivotal role in DA patency of full-term neonates. Administration of oral ibuprofen in 10 - 5 - 5 mg/kg schedule could not induce PDA closure in full-term neonates."

"ABSTRAKSepsis adalah disfungsi organ yang mengancam jiwa akibat gangguan regulasi pejamu sebagai respons terhadap infeksi. Renjatan sepsis adalah subset sepsis dengan abnormalitas sirkulasi, selular, dan metabolisme yang berkaitan dengan risiko kematian. Penelitian ini bertujuan untuk menilai peran ekokardiografi, biomarker kardiovaskular, fungsi ginjal dan saturasi oksigen vena sebagai prediktor kematian pasien renjatan sepsis. Pada pemeriksaan ekokardiografi dinilai fungsi diastolik E/e rsquo;, Fraksi Ejeksi Bilik Kiri, Indeks Kardiak, TAPSE, sedangkan biomarker kardiovaskular dinilai Troponin I dan NT Pro BNP, dengan disain penelitian kohort prospektif. Tempat penelitian di Rumah Sakit Umum Kabupaten Tangerang, Banten. Selama periode 2 tahun penelitian ada 111 pasien masuk dalam kriteria renjatan sepsis yaitu adanya infeksi, hipotensi MAP < 65 mmHg dan Laktat darah > 2 mmol/L. Pada hari pertama dan kelima dilakukan pemeriksaan ekokardiografi dan laboratorium darah pada semua pasien renjatan sepsis. Pada pengamatan selama 10 hari diperoleh pasien yang meninggal 64 58 dan yang hidup 47 42 . Rerata umur pasien 48 18 tahun. Analisis bivariat ditemukan Fraksi Ejeksi Bilik Kiri abnormal memiliki risiko kematian 1,6 kali dibanding normal RR 1,6; p = 0,034 . Biomarker Troponin I abnormal menunjukkan risiko kematian 1,6 kali dibanding normal RR 1,6; p = 0,004 . Pasien dengan gangguan fungsi ginjal memiliki risiko kematian 1,5 kali RR 1,5; p = 0,024 . Pasien dengan Troponin I abnormal dengan atau tanpa gangguan fungsi ginjal menunjukkan peningkatan risiko kematian, demikian pula pada pasien dengan Troponin I normal yang disertai gangguan fungsi ginjal. Hasil analisis multivariat menunjukkan prediktor kematian pasien renjatan sepsis adalah kadar Troponin I dan Fraksi Ejeksi Bilik Kiri RR 1,83; IK95 1,049 ? 3,215; p = 0,043 dan RR 1,99; IK95 1,009 ? 3,956; p = 0,047 Simpulan: Troponin I dan Fraksi Ejeksi Bilik Kiri merupakan prediktor kematian pasien renjatan sepsis. Kata kunci :Ekokardiografi, Kematian, NT Pro BNP, Renjatan Sepsis, Troponin I.

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ABSTRACTSepsis is a life threatening organ dysfunction caused by host regulation disorder in response to infections. Septic shock is a subset of sepsis with circulatory, cellular, and metabolic abnormalities associated with the risk of mortality. The aim of this study is to assess the role of echocardiography, cardiovascular biomarker, renal function and oxygen vein saturation as predictors of mortality in patients with septic shock. In this study, echocardiography examination including diastolic function E e 39 , Left Ventricle Ejection Fraction LVEF , Cardiac Index CI , and TAPSE, whereas cardiovascular biomarker Troponin I and NT Pro BNP were assessed. Research design of this study is cohort perspective. The study took place in Tangerang Regional General Hospital, Banten Province. During two years of research, there were 111 patients included in septic shock category, which indicated by the presence of infections, hypotension MAP 65 mmHg and serum lactate 2 mmol L. On the first and the fifth day, examinations on echocardiography and laboratory blood test were conducted on each patient of septic shock. During ten days of observation, 64 patients died 54 and 47 patients were survived 42 . The mean age of the patients was 48 18 years old. Bivariate analysis showed abnormal LVEF had 1.6 times higher mortality risk than normal RR 1.6 p 0.034 . Abnormal Troponin I biomarker showed 1.6 higher mortality risk, compared to normal RR 1.6 p 0.004 . The patients with kidney function disorder had 1.5 times higher mortality risk RR 1.5 p 0.024 . Patients with abnormal Troponin I with or without kidney function disorder showed increase in mortality risk. Normal Troponin I with kidney function disorder also increase in mortality risk. Multivariate analysis showed Troponin I and Left Ventricular Ejection Fraction as predictors of mortality in patients with septic shock RR 1.83 CI95 1.049 3.215 p 0.043 dan RR 1.99 CI95 1.009 3.956 p 0.047 In conclusion, Troponin I biomaker and Left Ventricular Ejection Fraction are predictors of mortality in patients with septic shock. Keyword Echocardiography, Death, NT Pro BNP, Septic Shock, Troponin I "