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Abstrak :
Renjatan merupakan kegawat-daruratan tersering pada anak. Laktat sering digunakan sebagai target keberhasilan resusitasi pada renjatan sepsis, namun sepertiga kasus renjatan pada anak tidak mengalami peningkatan kadar laktat alaktatemia . Penilaian laktat sebagai target keberhasilan resusitasi masih menjadi perdebatan. Penelitian sebelumnya menyimpulkan nilai bersihan laktat berkaitan dengan luaran pasien renjatan sepsis. Laktat dehidrogenase LDH -1, LDH-5 dan delivery oxygen DO2 berperan dalam metabolisme laktat dan menyebabkan kondisi alaktatemia dan hiperlaktatemia pada pasien renjatan anak. Penelitian ini bertujuan untuk mencari etiologi alaktatemia pada renjatan anak melalui pemeriksaan isoenzim LDH-1, LDH-5 dan DO2 selama proses resusitasi 6 jam. Penelitian ini adalah penelitian potong lintang pada 56 renjatan sepsis dan 44 hipovolemik berusia 1 bulan sampai 18 tahun di 4 rumah sakit umum. Pemeriksaan tekanan darah mean arterial pressure/ MAP, indeks jantung cardiac index, CI dan indeks tahanan vaskular sistemik systemic vascular resistance index, SVRI , DO2 dan pengambilan darah untuk pemeriksaan LDH-1 dan 5 dilakukan sebelum dan setelah resusitasi. Pada penelitian ini didapatkan usia terbanyak berada dalam rentang 1 ndash;59 bulan 56, dengan pasien yang datang dengan kondisi berat skor pediatric logistic organ dysfunction/PELOD-2 ge; 10 31, median kadar laktat jam ke-0 adalah 2,5 mmol/L. Angka kematian 20 . Proporsi hiperlaktatemia lebih tinggi secara bermakna p = 0,028 pada pasien renjatan dengan skor PELOD-2 ge; 10 71,9 . Tidak ada perbedaan bermakna isoenzim LDH-1, LDH-5 dan DO2 antara kelompok alaktatemia dan hiperlaktatemia. Tidak ada perbedaan bermakna MAP, CI, SVRI antar kelompok alaktatemia dan hiperlaktatemia. Tidak ada perbedaan bermakna luaran pasien berdasarkan nilai bersihan laktat. Simpulan: Pasien yang mengalami alaktatemia tidak terbukti aktivitas LDH-1 meningkat sedangkan pada hiperlaktatemia aktivitas LDH-5 meningkat. Kadar DO2 lebih tinggi pada kelompok alaktatemia dan lebih rendah pada hiperlaktatemia.

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Shock is the most common emergency condition in pediatric patients. Lactate levels have been used widely as resuscitation target in septic condition. Meanwhile, one third cases did not showed elevated lactate levels alactatemia . Lactate levels as a target for successful resuscitation is still being considered. Previous studies concluded lactate clearance has correlated with the septic shock patients outcome. Lactate dehydrogenase LDH 1, LDH 5 and delivery oxygen DO2 have an important role in lactate metabolism and causing alactatemia and hyperlactatemia in pediatric shock. The objectives of this study were to determine the alactatemia etiology in pediatric shock using isoenzyme LDH 1, LDH 5 and DO2 examination during 6 hours resuscitation. This was a cross sectional study done in 56 patients with septic shock and 44 patients with hypovolemia, within aged 1 month until 18 years old in 4 general hospitals. Mean arterial pressure MAP , cardiac index CI , and systemic vascular resistance index SVRI , DO2, LDH 1 and LDH 5 were done before and after resuscitation. This study found the most common age is in average 1 ndash 59 months 56 , proportion of patients who came with severe condition pediatric logistic organ dysfunction PELOD 2 score ge 10 was 31 , median of lactate levels in 0 hours was 2.5 mmol L. Death rate was 20 . Hyperlactatemia proportion was higher significantly p 0.028 in shock patients with PELOD 2 score ge 10 71.9. There was no differences in MAP, CI, SVRI values between alactatemia and hyperlactatemia groups. There was no differences in outcome based on lactate clearance. Conclusion Patients with alactatemia do not prove that their LDH 1 activity is increased while in hyperlactatemia, the activity of LDH 5 is increased. DO2 levels were higher in the alactatemia group and lower in hyperlactatemia group.

Abstrak :
Panduan resusitasi anak umumnya menganjurkan pemberian cairan dalam jumlah besar. Beberapa penelitian memperlihatkan bahwa penggunaan cairan yang agresif meningkatkan mortalitas. Penelitian pada hewan menunjukkan tekanan vena sentral yang tinggi memicu pelepasan atrial natriuretic peptide ANP , sementara penelitian invitro memperlihatkan ANP meluruhkan glycocalyx endotel vaskular dan meningkatkan permeabilitas endotel. ANP juga memicu vasodilatasi. Hemodilusi berpotensi menurunkan pasokan oksigen tubuh DO2 . Penelitian bertujuan untuk melihat pengaruh resusitasi cairan terhadap kadar ANP serum, peluruhan glycocalyx endotel vaskular, extravascular lung water index ELWI , mean arterial pressure MAP , kadar hemoglobin dan pasokan oksigen. Hewan model renjatan adalah 11 ekor Sus scrofa jantan, usia 6-10 minggu. Renjatan dilakukan dengan metode fixed pressure hemorrhage. Resusitasi pertama dilakukan dengan jumlah cairan sesuai darah yang dikeluarkan resusitasi normovolemik , dilanjutkan dengan 40 mL/kg resusitasi hipervolemik . Pengukuran hemodinamik dilakukan dengan PICCO. Serum ANP dan Syndecan-1, petanda peluruhan glycocalyx, dilakukan dengan teknik ELISA. Hasil penelitian menunjukkan terjadinya peningkatan ANP pasca resusitasi normovolemik p = 0,043 , yang kemudian menurun kembali dalam 30 menit. Peluruhan glycocalyx tidak terjadi. Perbedaan ELWI pada 60 menit pasca resusitasi secara statistik bermakna, dengan perbedaan 0,93 mL/kg 95 IK:0,19 -3,62 . Terdapat korelasi kuat antara SVRI dan CI pasca resusitasi hipervolemik r = -0,587 . Tidak ada perbedaan MAP pasca resusitasi normovolemik dan hipervolemik. Kadar hemoglobin pasca resusitasi hipervolemik lebih rendah daripada pasca resusitasi normovolemik p = 0,009 . Pasokan oksigen tubuh pasca resusitasi hipervolemik lebih tinggi daripada pasca resusitasi normovolemik p = 0,012 . Simpulan: Resusitasi cairan pada renjatan akibat perdarahan tidak mengakibatkan peluruhan glycocalyx endotel vaskular. Peningkatan ELWI amat terbatas. SVRI berkorelasi terbalik dengan CI. Tidak ada perbedaan MAP antara resusitasi normovolemik dan hipervolemik. Resusitasi hipervolemik menyebabkan hemodilusi yang diimbangi dengan peningkatan curah jantung. ...... Many pediatric guidelines recommend liberal fluid resuscitation, but recent studies showed that aggressive fluid resuscitation might increase mortality. Animal studies showed that high central venous pressure induced ANP secretion. Invitro studies showed convincing evidence that ANP induced glycocalyx shedding. ANP also induced vasodilatation through cGMP signal transduction pathways. Hemodilution due to a large amount of resuscitation fluid potentially decreasing oxygen delivery.The objectives of this study were investigating the effect of fluid resuscitation, in the animal model, with special concern on serum ANP, glycocalyx shedding indicate by serum Syndecan-1 , changes in extravascular lung water, systemic vascular resirtance and mean arterial pressure, hemoglobin level and oxygen delivery DO2 . The animal models were 11 male domestic pigs, 6 -10 weeks old. The shock was induced with fixed pressure hemorrhage method. Fluid resuscitation was done in 2 phases. On the first attempt, we replaced total numbers of blood that withdrawn normovolemic resuscitation . On the second attempt, we gave 40 mL/kg resuscitation fluids hypervolemic resuscitation . The hemodynamic measurements were done with PICCO. Serum ANP and Syndecan-1 were measure with ELISA method.We found that serum ANP increased after normovolemic resuscitation p = 0.043 and immediately back to base level in 30 minutes. Glycocalyx shedding did not occur. Extravascular lung water index minimally increased. There was a strong correlation between SVRI and CI at hypervolemic resuscitation r = -0.587 . There was no difference in mean arterial pressure between normovolemic and hypervolemic resuscitation. Hemoglobin level after hypervolemic resuscitation was lower than after normovolemic resuscitation p = 0.009 . Oxygen delivery was higher after hypervolemic resuscitation p = 0.012 .Conclusions: Hypervolemic resuscitation in this hemorrhagic shock model did not induce glycocalyx shedding, extravascular lung water index minimally increased. Systemic vascular resistance index negatively correlated to cardiac index. Fluid resuscitation may induce hemodilution, but oxygen delivery can be compensated by increasing cardiac output.