Tujuan: Penelitian ini bertujuan mengetahui profil trauma pada kehamilan di RSUPN Cipto Mangunkusumo Jakarta dan RSUD Dok II Jayapura.
Metode: Penelitian bersifat deskriptif observasional. Semua ibu hamil dengan trauma yang memeriksakan dirinya ke RSUPN Cipto Mangunkusumo dan RSUD Dok II tahun 2016-2018 dimasukkan sebagai subyek penelitian. Data demografis, obstetrik, karakteristik trauma, gejala dan temuan klinis, serta luaran ibu dan janin dianalisa secara deskriptif.
Hasil: Didapatkan 100 kasus trauma dari 7130 ibu hamil dalam penelitian ini. Berdasarkan ISS (Injury Severity Score), 76% subyek termasuk trauma derajat ringan, 20% derajat sedang, dan 4% derajat berat. Tiga mekanisme trauma terbanyak adalah jatuh (61%), kecelakaan lalu lintas (24%), dan kekerasan domestik (9%) dengan jenis trauma kontusio (82%) dan trauma superfisial (60%). Gejala klinis meliputi nyeri abdomen (60%), perdarahan pervaginam (13%), dan ketuban pecah (8%). Didapatkan 1 kasus syok, 2 kasus solusio plasenta, dan 2 kasus gawat janin. Luaran ibu baik, dengan 3% abortus, 3% seksio sesarea, 9% induksi pervaginam, dan 85% konservatif (di mana 91,8% kehamilan berhasil dipertahankan, 7,0% lahir prematur dan 1,2% abortus spontan). Luaran janin menunjukkan 1% lahir mati, 4% abortus, 10% lahir prematur, 7% lahir aterm, dan 78% konservatif.
Kesimpulan: Insidens trauma pada kehamilan pada penelitian ini sebesar 1.4%. Sebagian besar subyek termasuk kategori trauma derajat ringan (76%), disebabkan mekanisme jatuh (61%), dengan jenis trauma kontusio (82%) dan klinis nyeri abdomen (60%). Didapatkan 1% kasus syok, 2% solusio plasenta, 2% gawat janin, 4% abortus, dan 1% lahir mati, tanpa adanya mortalitas ibu. ISS (Injury Severity Score) dapat diterapkan untuk menilai derajat trauma ibu hamil, namun tidak menggambarkan luaran ibu maupun janin.
Objectives: This study aimed to determine the profile of trauma in pregnancy at RSUPN Cipto Mangunkusumo Jakarta and RSUD Dok II Jayapura.
Methods: This was a descriptive observational study. All pregnant women with trauma went to RSUPN Cipto Mangunkusumo and RSUD Dok II during 2016-2018 were included. Demographic and obstetrics datas, trauma characteristics, clinical findings, and all maternal and fetal outcomes were analysed.
Results: Of all 7130 pregnant women included, there were 100 trauma cases. Using ISS (Injury Severity Score), 76% subjects had mild trauma, 20% moderate trauma, and 4% severe trauma. Three main trauma mechanisms were fall (61%), motor vehicle accidents (24%), and domestic assaults (9%), with contusion (82%) and superficial trauma (60%). Clinical symptoms included abdominal pain (60%), vaginal bleeding (13%), and water broke (8%). There were 1 hypovolemic shock and 2 placental abruption cases, with 2 fetuses showing fetal distress. Maternal outcomes were good; with 3% abortion, 3% caesarean-section, 9% vaginal induction, and 85% conservative cases (of which 91.8% managed to continue the pregnancy, 7.0% had preterm labor, and 1,2% had spontaneous abortion). Fetal outcomes showed 1% stillbirth, 4% abortion, 10% preterm birth, 7% term birth, and 78% conservative pregnancy.
Conclusions: Incidence of trauma in pregnancy in this study is 1.4%. Most subjects have mild trauma (76%), caused by fall (61%), presented mostly with contusion (82%) and abdominal pain (60%). We reported no maternal mortality, 1% hypovolemic shock, 2% placental abruption, 2% fetal distress, 4% abortion rate, and 1% stillbirth. ISS can be applied to assess maternal trauma degree, but does not represent maternal or fetal outcomes.
"Pendahuluan: Preeklampsia diketahui sebagai sindrom spesifik kehamilan dan salah satu penyebab tersering kematian ibu. Terdapat dua jenis preeklampsia, awitan lambat dan awitan dini. Akan tetapi, penelitian menujukkan bahwa preeklampsia awitan dini jauh lebih berbahaya untuk ibu dan bayi. Meskipun patogenesis preeklampsia masih belum jelas, insufisiensi plasenta akibat meningkatnya peroksidasi lipid dan invasi trofoblas yang defektif diduga sebagai salah satu faktor pencetus preeklampsia. PPARg, yang berfungsi untuk metabolisme lipid dan diferensiasi sel di plasenta, secara teori dapat mencetuskan preeklampsia apabila aktivasinya berkurang. Dengan demikian, studi ini ditujukan untuk menganalisis secara spesifik ekspresi protein PPARg pada plasenta preeklampsia awitan dini. Selain itu, analisis terhadap ekspresi protein PPARg juga dilakukan berdasarkan kategori karakteristik subjek, yaitu usia ibu dan usia kehamilan.
Metode: Penelitian ini merupakan studi deskriptif potong lintang. Sebanyak 26 sampel jaringan plasenta dengan usia gestasi ≤ 33 minggu (preeklampsia awitan dini) digunakan dalam penelitian ini. Konsentrasi protein PPARg diukur pada homogenat jaringan plasenta dengan menggunakan metode ELISA. Selanjutnya, analisis data dilakukan secara statisik mennggunakan perangkat lunak IBM SPSS Statistics. Varian tes yang digunakan adalah t-test dan Mann-Whitney test untuk perbandingan, serta Pearson dan Spearman untuk tes korelasi.
Hasil: Ekspresi PPARg adalah 3.19±1.13 ng/mg protein; usia ibu 29.65±5.97 tahun; usia gestasi 30.50 (24-33) minggu. Berdasarkan kategori usia ibu, usia <30 tahun mengekspresikan PPARg sebesar 2.81 (0.60 – 5.71) ng/mg protein, sedangkan usia ≥30 tahun mengekspresikan 3.17 (1.75 – 5.40) ng/mg protein. Pada kategori usia gestasi, usia <30 minggu mengekspresikan PPARg sebanyak 2.86±1.14 ng/mg protein PPARg dan usia ≥30 minggu sebanyak 3.48±1.07 ng/mg protein. Dibandingkan dengan plasenta kehamilan normal (3.52 (1.12 – 12.43) ng/mg protein), plasenta preeklampsia mengekspresikan 2.94 (0.60 – 5.71) ng/mg protein PPARg.
Kesimpulan: Konsentrasi PPARg yang lebih tinggi ditemukan pada wanita berusia ≥30 tahun daripada wanita berusia <30 tahun. Berdasarkan usia gestasi (UG), konsentrasi PPARg pada UG ≥ 30 minggu lebih tinggi dibandingkan UG < 30 minggu. Jika dibandingkan dengan plasenta kehamilan normal, plasenta preeklampsia memiliki konsentrasi PPARg yang lebih rendah.
Introduction: Preeclampsia is regarded as a specific pregnancy disorder and one of the leading causes of maternal death. There are two types of preeclampsia, late-onset and early-onset. However, evidences have proven that early-onset preeclampsia is associated to deleterious outcomes for both mother and newborns. Though the pathogenesis is still unclear, placental insufficiency due to increased lipid peroxidation and defective trophoblast invasion is thought to be one cause of preeclampsia. PPARg, which functions for lipid metabolism and cell differentiation in placenta, is correlated to preeclampsia once the activation is lessened, theoretically. Thus, this research was intended to analyse protein expression of PPARg, specifically in placenta of early-onset preeclampsia. In addition, the analysis also conducted according to characteristics of the subjects, which are maternal age and gestational age.
Methods: The design of this research was descriptive cross-sectional study. There are 26 samples of placental tissues used with gestational age ≤ 33 weeks (early onset preeclampsia). In form of placental homogenates, protein concentration of PPARg was measured by using ELISA method. Statistical data analyses was performed in IBM SPSS Statistics software by using t-test and Mann-Whitney test for comparison, also Pearson and Spearmen for correlation test.
Results: The expression of PPARg was 3.19±1.13 ng/mg protein; maternal age 29.65±5.97 years; gestational age 30.50 (24-33) weeks. PPARg expression according to maternal age category is 2.81 (0.60 – 5.71) ng/mg protein in <30 years and 3.17 (1.75 – 5.40) ng/mg protein in ≥30 years. Based on gestational age (GA) group, GA <30 weeks expresses 2.86±1.14 ng/mg protein PPARg, while GA ≥30 weeks shows 3.48±1.07 ng/mg protein PPARg. In comparison to normal placenta (3.52 (1.12 – 12.43) ng/mg protein), preeclamptic placenta expresses 2.94 (0.60 – 5.71) ng/mg protein PPARg.
Conclusion: Distribution of PPARg is established higher in women aged ≥30 years than women aged <30 years. In gestational age ≥30 weeks, the PPARg distribution is also higher compared to gestational age <30 weeks. However, preeclamptic placenta distributes lower amount of PPARg than normal placenta.
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