KONSEP KEPERAWATAN GAWAT DARURAT(GADAR)


KEPERAWATAN GAWAT DARURAT (KEGAWAT DARURATAN & KEKRITISAN) : FILOSOFI, KONSEP HOLISTIK & PROSES KEPERAWATAN

A. DEFINISI KGD :
Pelayanan profesional yg didasarkan pada ilmu keperawatan gawat darurat & tehnik keperawatan gawat darurat berbentuk pelayanan bio-psiko-sosio- spiritual yang komprehensif ditujukan pada semua kelompok usia yang sedang mengalami masalah kesehatan yang bersifat urgen , akut dan kritis akibat trauma, proses kehidupan ataupun bencana.
B. MATA AJAR KEPERAWATAN GAWAT DARURAT
AREA : Pra Rumah sakit dan Rumah sakit
KEMAMPUAN :Pengetahuan, Sikap & ketrampilan u/ memberikan ASKEP kegawatan & Kekritisan khususnya hal-hal yg terkait LIVE SAVING.
C. LINGKUP BAHASAN :
a. Konsep dasar KGD
b. Sisitem pelayanan KGD pra RS, Uit Gawat Darurat & prw Intensif.
c. Perawatan klien semua tk usia dng kegawatan sist : pernafasan, kardiovaskuler, persyarafan, pencernaan & endokrin, perkemihan, muskuloskeletal, reproduksi, jiwa & psikiatri
D. EMERGENCYNURSING ( KEPERAWATAN KRISIS )
a. DEFINISI EN : Sebuah area khusus / spesial dr keperawatan profesional yg melibatkan integrasi dari Praktek, Penelitian, Pendidikan profesional.
b. Praktek keperawatan emergency oleh seorang perawat profesional
c. FOCUS : Memberikan pelayanan secara episodik kpd pasien-pasien yg mencari terapi baik yg mengancam kehidupan , non krotical illness atau cedera.
d. INTI : Ditujukan pd esensi dr praktek emergency, lingkungan dimana hal tsb terjadi dan konsumen-konsumen keperawatan emergency.
e. EMERGENCY NURSES : RN profesional yg memiliki komitmen u/ menyelamatkan dan melaksanakan praktek keperawatan scr efektif.



E. EMERGENCY CARE
Pengkajian, diagnosis & terapi kep. yg dpt diterima baik aktual, potensial, tjd tiba-tiba atau urgen, masalah fisik atau psikososial dalam episodik primer atau akut yg mungkin memerlukan perawatan minimal atau tindakan support hidup, pendidikan u/ pasien atau orang terpenting lainnya, rujukan yg tepat dan pengetahuan ttg implikasi legal.
F. EMERGENCY CARE ENVIRONTMENT
Setting dimana pasien memerlukan intervensi oleh pemberi pelayanan kep emergency.
G. EMERGENCY PATIENT
1. Pasien dr segala umur dng diagnosa, tidak terdiagnosa atau maldiagnosis problem dng kompleksitas yg bervariasi.
2. Pasien-pasien yg memerlukan intervensi nyata dimana dpt terjadi perubahan status fisiologis atau psikologis scr cepat yg mungkin mengancam kehidupannya.
H. DIMENSI
Multidimensi meliputi : RESPONSIBILITIES, FUNCTION, ROLES, SKLILLS ( dng pengetahuan khusus )
1. KARAKTERISTIK UNIK PRAKTEK KEP. GADAR
a. Pengkajian, diagnosa, terai baik yg urgen / non urgen individual dari berbagai umur pasien walaupun dng data / informasi yg sangat terbatas
b. Triage & Prioritas
c. Persiapan bencana alam
d. Stabilisasi & resusitasi
e. Krisis intervensi u/ populasi ps yg UNIk spt korban kekerasan sexual
f. Pemberian perawatan pd lingkungan yg tidak terkontrol atau yg tidak dpt diprrediksikan
2. KERANGKA KERJA PROSES KEP. EN
a. TUJUAN
• Menyelamatkan hidup
b. PENGKAJIAN
 Pada sistem yg terganggu
 U/ memperbaiki kegagalan atau mempertahankan sistem
c. DIAGNOSIS
 Mencari perbedaan u/ menemukan tanda-tanda & gejala
d. PERENCANAAN
 Berdasarkan protokol dan prosedur
e. INTERVENSI
 Terapi ditujukan pd penanganan gejala krisis & stabilisasi ps.
 Diteruskan s/d pasien stabil u/ dpt pindah atau ditransportasikan ke unit lain atau meninggal




PERTOLONGAN PERTAMA PADA GIGITAN ULAR

A. Ular berbisa di Indonesia
Ular berbisa hanya sedikit yang ditemukan di Indonesia, diantaranya: ular sendok (kobra), ular anang (tedung atau king kobra), ular welang, ular weling, ular hijau pucuk/ular gadung (luwuk), ular taliwangsa (belang hitam-kuning) dan ular tanah (coklat tua dengan taring panjang).

B. Sifat Ular
Sifat ular yang harus dipahami adalah; ular takut pada manusia, menggigit untuk memperingatkan/mengusir manusia (pada kebanyakan kasus) serta 70% gigitan ular bukan dari ular berbisa, umumnya hanya sedikit atau tidak ada racun yang disuntikkan. Gigitan ular tidak semuanya berakhir dengan kematian. Kematian tidak datang seketika atau dalam beberapa menit saja. Gejala biasanya timbul 15 menit sampai 2 jam kemudian setelah korban digigit ular.

C. Ciri-ciri ular berbisa
Ciri secara umum (tidak mutlak) yg biasanya ada pada ular berbisa, yaitu: bentuk kepala pipih dan berpola huruf ‘V’, ukuran relatif kecil atau pendek, kecuali King Cobra yang bisa mencapai 5 meter dan warna biasanya cerah (tetapi hal ini tidak mutlak).

D. Mencegah tidak digigit ular
Mencegah agar tidak digigit ular adalah; jangan membuat koleksi dari ular, tinggalkan/jangan ganggu ular. beberapa orang digigt karena berusaha membunuh atau mencoba mendekat. Di daerah yang banyak ular, pakai sepatu, kaos kaki dan jeans apabila keluar rumah , jangan masukkan tangan dicelah-celah timbunan kayu atau sampah, Bila berjalan di semak belukar usahakan membuat suara berisik agar ular tahu keberadaan kita dan menyingkir, hati-hati bila berjalan di rumput yang tebal dan potong pendek rumput di sekitar rumah, tempat kerja dan sekolah dan pergunakan senter bila berjalan di malam hari.

E. gambaran gigian ular berbisa
Gambaran gigian ular berbisa akan timbul rasa nyeri daerah tusukan (muncul segera seelah gigitan), daerah gigitan bengkak, kemerahan, memar (dapat cepat berkembang), reaksi emosi yang kuat, penglihatan kembar/kabur, mengantuk, sakit kepala, pusing dan pingsan, mual dan atau muntah dan diare, rasa sakit atau berat didada dan perut, tanda-tanda tusukan gigi, gigitan biasanya pada tungkai/kaki, sukar bernafas dan berkeringat banyak, kesulitan menelan serta kaku di daerah leher dan geraham.

F. Pertolongan pertama
pertolongan pertama, pastikan daerah sekitar aman dan ular telah pergi segera cari pertolongan medis jangan tinggalkan korban. selanjutnya lakukan prinsip :
R = Reassure = yakinkan kondisi korban, tenangkan dan istirahatkan korban,
kepanikan akan menaikan tekanan darah dan nadi sehingga racun akan lebih cepat
menyebar ke tubuh. terkadang pasien pingsan / panik karena kaget.
I = Immobilisation = jangan menggerakan korban, perintahkan korban untuk tidak
berjalan atau lari. Jika dalam waktu 30 menit pertolongan medis tidak datang:
lakukan tehnik balut tekan ( pressure-immoblisation ) pada daerah sekitar gigitan
(tangan atau kaki) lihat prosedur pressure immobilization (balut tekan)
G = Get = bawa korban ke rumah sakit sesegera dan seaman mungkin.
T =Tell the Doctor = informasikan ke dokter tanda dan gejala yang muncul pada
korban.

G. Prosedur Pressure Immobilization (balut tekan)
1. Balut tekan pada tangan
a. Istirahatkan (Immobilisasikan) Korban
b. Keringkan sekitar luka gigitan
c. Gunakan pembalut elastis
d. Jaga luka lebih rendah dari jantung
e. Sesegera mungkin, lakukan pembalutan dari bawah pangkal jari kaki naik keatas.
f. Biarkan jari kaki jangan dibalut
g. Jangan melepas celana atau baju korban
h. Balut dengan cara melingkar cukup kencang namun jangan sampai menghambat
aliran darah (dapat dilihat dengan warna jari kakiyang tetap pink)
i. Beri papan/pengalas keras sepanjang kaki.

2. Balut tekan pada tangan
a. Balut dari telapak tangan naik keatas. ( jari tangan tidak dibalut)
b. Balut siku & lengan dngn posisi ditekuk 90 drjt.
c. Lanjutkan balutan ke lengan s/d pangkal lengan.
d. Pasang papan sebagai fiksasi
e. Gunakan mitela untuk menggendong tangan

H. Kesalahan Penanganan
Kesalahan penanganan yg sering dilakukan, mengikat (Tourniquets) sekitar luka /gigitan membuat sayatan memotong, membuat perdarahan atau menggerakan daerah gigitan, mencuci luka gigitan dan menyedot racun dari luka gigit
I. Pertolongan di RS
1. Pasang I.V.,
2. resusitasi cairan jika diperlukan
3. Pelacakan alergi,
4. Jenis gigitan untuk menentukan antibisa
5. Resusitasi kardiopulmoner jika diperlukan,
6. Adrenalin
7. Cek laboratorium darah, jika dlm waktu 4 jam darah korban tidak terdapat tanda
koagulopati, miolisis dan pasien tidak menunjukan tanda gigitan berbisa maka pasien
tidak terkena gigitan berbisa.

J. Penatalaksanaan gigitan ular berbisa
1. Infus RL,
2. resusitasi cairan jika diperlukan
3. Cek laboratorium
4. Urinalisa
5. Darah lengkap
6. Golongan darah
7. Ptt,aptt, fibrinogen
8. BUN, creatinin, Va, phospat, dll
9. EKG
10. Monitor ketat pasien ( tiap 15mnt – 2 jam setelah gigitan )
11. Intubasi jika gagal nafas, cek sumbatan jalam nafas
12. RKP jika cardipulmonary arrest
13. pemberian antibisa
14. Larutkan antibisa dalam RL 60 cc,
15. berikan selama 30 mnt
16. Cek efek antibisa 15 menit setelah antibisa habis
17. Kemudian buka balutan dng hati-hati dlm waktu 5 mnt,
18. Jika setelah dibuka keadaan umum pasien tambah buruk
19. lakukan pembidaian kembali
20. Beri ATSAntibiotik profilaksis
21. Kontraindikasi diberikan Morfin



KASUS TRAUMA ABDOMEN

A. kasus
Pria (25) ditendang di daerah perut saat berkelahi. Shg mengalami hematoma dan abrasi, ttp petugas medis tdk melihatnya sbg cedera yg serius, diberi aspirin dan dipulangkan. 3 hari kmdn masuk RS dgn peritonitis berat. Sejumlah besar pus dan isi usus dikeluarkan ttp tak lama kemudian meninggal
B. Pendahuluan
Trimodal Death Distribution
KLL >> multiple trauma
85 % Multiple trauma >> Trauma abdomen
Angka Kematian trauma abdomen ??
C. Anatomi
• Batas rongga Abdomen :
a. Atas : Diafragma
b. Bawah : Pelvis
c. Depan : Dinding depan abdomen
d. Lateral : Dinding lateral abdomen
e. Belakang : Dinding belakang abdomen serta tulang belakang
D. Anatomi abdomen
E. Organ Abdomen
a. Solid
b. Berongga
F. Topografi Abdomen
a. Intra peritoneal
b. Retro peritoneal
c. Pelvical
G. Trauma Abdomen
• Trauma Tumpul
a. Benturan langsung, Setir mobil, stang
b. Ruptur organ >> Uterus bumil
c. Shearing Injuries >> penggunaan sabuk pengaman yg salah
d. Deceleration
• Trauma Tembus
a. Luka tusuk
b. Luka tembak kecepatan rendah >> kerusakan jaringan, lacerasi, putus
c. Luka tembak kecepatan tinggi >> hancur organ dalam
• Trauma penetrasi
a. Trauma penetrasi
H. mekanisme
Mechanism of injury?
Mekanisme Trauma ?
I. Pengkajian
• Riwayat trauma ? Biomekanika trauma?
• Pemeriksaan fisik abdomen :
a. Inspeksi
b. Auskultasi
c. Perkusi
d. Palpasi
J. Pemeriksaan
a. Stabilitas pelvis
b. Penis, perianal, rectal, vagina ?
c. Gluteal
K. Pemasangan kateter
a. Gastric tube :
• Mengurangi dilatasi akut lambung
• Dekompresi sebelum dilakukan Diagnostic Peritoneal Lavage (DPL)
• Mengeluarkan isi lambung >> resiko aspirasi >>>> bila ada darah ??
b. Kateter urine :
• Mengurangi retensi urine
• Dekompresi VU sebelum dilakukan DPL >>>>darah pada meatus ??
L. Pengambilan sampel
a. Darah
b. Urine
M. Pemeriksaan radiologis
a. Foto polos abdomen
b. Dengan kontras :
• uretrografi
• Cystografi
• IVP
N. Emergency Management
a. ABC
b. Cegah shock & infeksi
c. Jangan berikan apapun melalui mulut
d. Jangan sentuh bagian eviscerasi, lakukan penutupan luka seperti pada gambar
e. Jangan ambil impaled objects, lakukan fiksasi pada benda tersebut.
f. Monitoring ketat :
• Tingkat kesadaran
• Tanda vital >> hipotensi
• Adanya peritonitis
• Serial Hb
g. Segera rujuk / transportasi untuk Tindakan definitif.
O. Prosedur khusus
a. Diagnostic Peritoneal Lavage > memasukkan kateter pd peritoneal :
• multiple trauma
• hemodinamik tak stabil
• DPL Positif bila :
• Bila ada darah, isi usus, serat sayuran, cairan empedu
• Analisis kuantitatif cairan pencuci positif bila:
 RBC >100.000/mm3
 WBC > 500/mm3
 Hematocrit >2 ml/dl
b. laparatomi !!
a. Indikasi laparatomi
b. Trauma tumpul abdomen DPL positif
c. Trauma tumpul abdomen dg hipotensi berulang
d. Peritonitis akut
e. Hipotensi dengan luka tembus abdomen
f. Perdarahan gaster, rectal, daerah genitourinari akibat trauma tembus
g. Indikasi…...
h. Luka tembak melintas peritoneum/retroperitoneum viseral/vaskular
i. Eviscerasi
j. Rontgen :
 ada udara bebas rongga peritoneum, ruptur diafragma
 CT : ruptur GI tract, cedera kandung kemih, renal dan organ vital lain.
P. Ringkasan
a. Trauma abdomen bisa disebabkan oleh trauma tumpul dan trauma tajam
b. Fokus tindakan emergency :
• ABC
• Cegah shock
• Cegah infeksi
• Monitoring.


KEGAWATAN OBSTETRIK

I. Emergency Obstetric Care
A. Pendahuluan
Maternal mortality claims 514,000 women’s lives each year. Nearly all these lives could be saved if affordable, good-quality obstetric care were available 24 hours a day, 7 days a week.
B. Pengertian
Kasus obstetri yg apabila tidak segera ditangani akan berakibat kematian ibu dan janinya . Kasus ini sbg penyebab kematian ibu, janin dan bayi baru lahir. Obstetrical emergencies are life-threatening medical conditions that occur in pregnancy or during or after labor and delivery.
C. Penyebab utama kematian :
Most of the deaths are caused by haemorrhage, obstructed labour, infection (sepsis), unsafe abortion and eclampsia (pregnancy-induced hypertension). Indirect causes likemalaria, HIV and anaemia

D. KASUS PERDARAHAN
1. Abortus
2. Kehamilan ektopik terganggu
3. Mola hidratidosa
4. Placenta previa
5. Abruptio placenta
6. Inversi atau Ruptur uteri
7. Atonia uteri
8. Ruptur perineum & robekan dinding vagina
9. AMNIOTIC FLUID EMBOLISM
10. Retensio plasenta
11. rolapse of the umbilical cord
12. Shoulder dystocia
E. INFEKSI & SEPSIS
1. Infeksi dlm kehamilan:
a. Virus varicella,
b. influenza,
c. toksoplasmosisherpes genitalia
2. Infeksi dlm persalinan:
a. korioamnionitis
3. Infeksi nifas :
a. metritis,
b. tromboplebitis
F. MANIFESTASI KLINIS
Untuk masing-masing ksus berbeda dng rentang waktu yg luas, perdarahan dpt bermanifestasi dari perdarahan berwujud bercak merembes profus s/d shockInfeksi & sepsis, bermanifestasi mulai dr pengeluaran cairan pervaginam yg berbau, air ketuban hijau, demam s.d shock. Pre eklamsi & eklamsi, mulai dr keluhan sakit kepala / pusing, bengkak, penglihatan kabur, kejang-kejang, tidak sadar s/d koma
G. Diagnosis
In a hospital or other urgent care facility. patient's medical history and perform a pelvic and general physical examination.The mother's vital signs, if preeclampsia is suspected, blood pressure may be monitored over a period of time. The fetal heartbeat is assessed with a doppler stethoscope, and diagnostic blood and urine tests: protein and/or bacterial infection.
An abdominal ultrasound: malpositioned placenta, such as placenta previa or placenta abruption.

II. KEHAMILAN EKTOPIK TERGANGGU (KET)
A. DEFINISI
KET adalah kehamilan dimana setelah fertilisasi , implantasi terjadidiluar endometrium kavum uteri.KET dpt mengalami abortus atau ruptur apabila masa kehamilan berkembang melebihi kapasitas ruang implantasi dan peristiwa ini disebut sbg KET
B. TANDA & GEJALA
1. Gejala kehamilan muda & abortus imminens
2. Pucat / anemia
3. Keadaan umum lemah, terjadi penurunan lesadaran
4. Shock
5. Nyeri tekan
6. Nyeri perut bagian bawah yang makin hebat apabila tubuh digerakan
C. PENANGANAN KET
1. Pemeriksaan fisik, tes kehamilan, anamnesa untuk menegakan diagnosa KET
2. Setelah terdiagnosa KET, segera lakukan persiapan operasi gawat darurat
3. Sediakan darah
4. Upayakan stabilisasi pasien dengan terapi cairan
5. Kendalikan nyeri pasca tindakan konseling pasca tindakan .

III. RUPTUR UTERI , Ruptur uteri merupakan komplikasi yg sangat fatal
A. DEFINISI
Robekan dinding rahim akibat dilampauinya daya regang miometrium yang disebabkan oleh disproporsi janin dan panggul, partus macet atau traumatik
B. TANDA & GEJALA KLINIS
1. Didahului oleh lingkaran konstriksi ( Bandl’s ring) hingga umbilikus atau diatasnya
2. Nyeri hebat pada perut bagian bawah
3. Hilangnya kontraksi & bentuk normal uterus gravidus
4. Perdarahan pervaginam dan shock
C. PENANGANAN RUPTUR UTERI
Penanganan dan pengenalan segera dan tepat pada kasus ini dapt menyelamatkan pasien dari kematian
1. Tindakan paling tepat : operasi laparatomi u/ menlahirkan anak & placenta
2. Resusitasi cairan untuk mengganti kehilangan darah
3. Pantau tanda vital & shock hipovolemik scr ketat
4. Bila konsenvasi uterus masih diperlukan & kondisi jaringan memungkinkan, dilakukan tindakan operasi uterus
5. Bila luka mengalami nekrosis luas & kondisi pasien menghawatirkan dilakukan histerektomi
6. Pemantauan ketat KU, TV, perdarahan, kesadaran, shock, lab dll , pasca operasi




IV. ABRUPTIO PLACENTA
A. DEFINISI
Suatu keadaan dimana plasenta terlepas dari dinding dalam uterus sebelum bayi lahirMerujuk pada terlepasnya plasenta yg terletak pada posisi normalnyan setelah minggu ke 20 kehamilan dan utamanya pada saat kelahiran.
B. Statistik
Prev di dunia sekitar 1% dari seluruh kehamilan di dunia.
C. Mortalitas/mordibitas:
Kematian IBU dan JANIN dapat terjadi krn PERDARAHAN dan KOAGULOPATI.
Kematian bayi stlh lahir sekitar 15%
D. Klasifikasi
Berat ringanya komplikasi abruptio placenta tergantung pada : jumlah perdarahan, derajat lepasnya placenta, ukuran bekuan darah yang terbentuk pada permukaan placenta maternal.
Ada beberapa sistem pengklasifikasian derajat abruptio placenta, salah satunya adalah dng pembagian :
1. RINGAN
<> 2/3 bagian placenta terlepas dr uterus yang menyebabkan kaku & kencangnya uterus terus-menerus yang disertai nyeri berat. Perdarahan hitam pervaginam + ( > 1000 cc ), terkadang perdarahan tidak terjadi. Distres fetus mulai terjadi dan jika fetus tidak dilahirkan kematian tidak dpt dielakan. Terlepasnya plasenta menyebabkab ibu mengalami shock, kematian fetus, nyeri hebat dan kemungkinan berkembangnya DIC ( disseminated intravaskular coagulation )
E. Causes
1. Perdarahan retroplasenta karena penusukan jarum
2. Hamil pada usia tua
3. idiopatik
4. Fibromioma retroplacenta
5. Hipertensi maternal
6. Maternal trauma
7. Ibu perokok
8. Penggunaan kokain
9. Tali pusat pendek
10. Dekompresi pd uterus yg tiba-tiba
F. FAKTOR PREDISPOSISI
1. Kondisi yg berhubungan dng abruptio placenta :
2. PIH ( pregnancy induced hypertension ) atau hipertensi kronik (140 / 90 mmhg )
3. Ruptur prematur dari membran <> 35 th, anomali uterus fibroid dan penyakit vaskuler misalnya DM atau penyakit colagen. Trauma eksternal ( misal kecelakaan )
4. Resiko akibat perilaku misalnya merokok, mengkonsumsi ethanol, kokain, methemphetamin
5. Riwayat abruptio placenta
6. Dekompresi cepat dr distensi yg berlebihan misal pd gestasi ganda, polihidramnion
7. Defisiensi asam folat ( jarang terjadi )
8. Riwayat
9. Ps biasanya memperlihatkan gejala :
10. Perdarahan Vaginal (80%)
11. Nyeri Abdomen / back pain dan kekakuan uterus (70%)
12. Fetal distress (60%)
13. Kontraksi abdomen Abnormal (hipertonik, frek tinggi) (35%)
14. Idioaphic prematur labor (25%)
15. Kematian Fetus (15%)
G. TANDA & GEJALA
1. Sangat tergantung pd luas / jumlah plasenta yg
2. lepas dan tipe abruptio
3. Sangat bervariasi
4. Tanda klasik kejadian akut “ knife like “ abdominal pain dng atau tanpa perdarahan pervaginam
5. AP ringan, gejalanya dpt spt nyeri melahirkan
6. AP berat nyeri dpt terjadi tiba-tiba & spt ditusuk pisau
7. Jika tjd perdarahan abdomen mjd membesar & uterus kaku. Abdomen spt “ board-like”
8. A couvelaire uterus s/d shock pd ibu
9. Perdarahan pervaginam ( pd 80% penderita )
10. Fetal distres s/d meninggal
H. Uji diagnostik
1. Lab
• Hb
• Ht
• Platelet
• Prothrombin/ aptt
• Fibrinogen
• Fibrin
• D-dimer
• Gol darah
2. USG
• Prehospital management
• Mon TV kontinyu
• O2 kontinyu-high flow
• IV line (1-2 jalur ): NaCl / RL
• Mon perdarahn vagina
• Mon DJJ
• Terapi shock jk diperlukan
3. ED
• Observasi ketat
• O2 tinggi
• DJJ mon
• IV-cairan
• Resusc cairan K?P
• Mon TV- U/O
• PRC- 4 unit disiapkan
• Mon penurunan tekanan intrauterin
• Seceparnya operasi SC
• Kolaborasi terapi DIC
I. PENATALAKSANAAN
Bervariasi tergantung : umur gestasi fetus, beratnya abruptio, komplikasi yg berhubungan, status ibu & fetus.
1. jk perdarahan banyak & tidak dpt dikontrol dilakukan persalinan yg tepat
2. Penentuan persalinan cepat tergantung pd beratnya abruptio placenta dan janin hidup / mati
3. AP berat dng atau tanpa perdarahan pervaginam dilakukan operasi sesar
4. Kehamilan dibawah 37 minggu penatalaksanaanya diyujukan pd memperpanjang kehamilan dengan harapan maturitas fetus
5. Jika fetus immatur dan tidak memperlihatkan kompresi fetus serta perdarahan pd ibu tidak menyebabkan hipovolemiadilakukan observasi ketat scr dini.
6. Fungsi koagulasi & status vilume obu baik tp terdapat distress fetus persalinan dilakukan dng cara yg aman.
V. PRE EKLAMSI & EKLAMSI
A. PRE EKLAMSI
Diagnosa pre eklamsi didasarkan pd berkembangnya pregnancy- induced hypertension dengan proteinuria, edema atau keduanya setelah 20 minggu kehamilan. Pre eklamsi dpr diklasifikasikan berat jika terdapat satu atau lebih gejala dibawah ini :
1. Pd keadaan istirahat TD sistolik ³ 160 mmhg atau diastolik 110 mmhg yg terjadi dua kali minimal dlm waktu 6 juam.
2. Proteinuria ³ 5 gr / 24 jam
3. Oliguria <> disukai IV , loading dose 4 mg dilanjutkan IV 1 - 2
2. KONTROL TEKANAN DARAH
tujuan terapi adalah menurunkan tekanan darah sistemik sapai pd titik dimana ststua ibu stabil. Tidak harus menurunkan sampai normal.
3. TERAPI SUPPORTIF
Pada pre eklamsi berat sering terjadi edema paru cadiac dan noncardiac. Terapi olsigen diberikan u/ mempertahankan PaO2 > 70 mmhg u/ mempertahankan oksigenasi fetus. K/P intubasi challengec cairan IV sebaiknya diberikan. Jk tidak berhasil lakukan monitoring hemodinamik invasif. Jk IV volume adekuat terapi vasodelator dpt membantu, monitoring ketat tanda vital, hemodinamik,status neurologis, kondisi janin, oksigenasi, dll.
4. HELLP SYNDROME
a. H = HEMOLISIS, an abnormal peripheral smear, total bilirubin > 1,2 mg/dl, atau kadar serum lactat dehydrogenase ( LDH ) > 600 U/L
b. EL=elevated lever enzym, aspartate aminotransferase ( AST) > 70 U/L atau LDH > 600U/L dan
c. LP= low platelet count - < 100,000/mm3
• Mengidentifikasi adanya kondisi kehamilan yg BERAT & MENGANCAM KEHIDUPAN
• Variasi sindroma ini mungkin tida melibatkan seluruh gejala diatas. Dapat muncul dng tanda yang tidak spesifik seperti nyeri epigastrum atau nyeri kuadran kanan bawah, malaise, mual, muntah,.
• Umumnya terjadi pada usia kehamilan 27 – 36 mg.
• pre eklamsi / eklamsi umumnya mendahului HELLP syndrome tapi 1/3 ps tidak mengalami hipertensi.
• Merupakan bagian dari fibrolisis atau hemolisis dr pre eklamsi trombositopenia DIC, perdarahan ntraserebral, gagal ginjal,
• Terkadang gejalanya dikacaukan dengan acute fatty liver in pregnancy
• Tidak merupakan indikasi persalinan namun demgan meningkatnya mordibitas fetus & maternal diperlukan persalinan yg tepat. Terapi hampir sama dengan pre eklamsi berat / eklamsi.
VI. AMNIOTIC FLUID EMBOLISM
A rare but frequently fatal complication of labor occurs when amniotic fluid embolizes from the amniotic sac and through the veins of the uterus and into the circulatory system of the mother. The fetal cells present in the fluid then block or clog the pulmonary artery, resulting in heart attack. This complication can also happen during pregnancy, but usually occurs in the presence of strong contractions.
VII. PROLAPSED UMBILICAL CORD
A prolapse of the umbilical cord occurs when the cord is pushed down into the cervix or vagina. If the cord becomes compressed, the oxygen supply to the fetus could be diminished, resulting in brain damage or possible death.
VIII. SHOULDER DYSTOCIA
Shoulder dystocia occurs when the baby's shoulder(s) becomes wedged in the birth canal after the head has been delivered.


INTOKSIKASI
Penyebab intoksisasi ada banyak macam, yang sering terjadi adalah karena kecelakaan atau, disengaja / bunuh diri. Di Amerika intoksikasi ± 75% terjadi pada anak umumnya karena keracunan produk rumah tangga

A. Agen Intoksikasi
Terjadi pada semua umur remaja: obat-obat psikotropik, sedative, transqualizer, antidepresan dan obat-obat narkotik. dewasa umumnya karena kecelakaan kerja (karbon monoksida, pestisida, keracunan makanan, dll)

B. Mekanisme
Mekanisme cidera masing-masing racun memiliki efek patologis yang berbeda-beda dimana masing masing racun memiliki patologi sendiri-sendiri. Efek racun dapat terjadi pada tempat atau sekitar masuknya racun (misalnya reaksi kimia sitotoksin) dan dapat berupa toksisitas sistemik yaitu efek-efek selektif racun atau efek metabolik khusus dari racun itu terhadap target yang spesifik misalkan asetaminofen di liver, methanol diretina, dll.

C. Pengkajian Prioritas Utama
1. Pengkajia riwayat kejadian, tanyakan pada pengantar pasien/pasien sendiri jika kooperatif.
2. Pengjakian fisik : Initial assessment/ Arway- Breathing- Cirkulating ( ABC)
a. Tingkat kesadaran
b. Pernafasan dan efektifitas nafas
c. Irama jantung
d. Ada tidaknya kejang
e. Keadaan dan warna kulit
f. Besar dan reaksi pupil mata
g. lesi, bau mulut, dan lainnya
Terkadang setelah mendapatkan resusitasi (ABC) sering dilanjutkan dengan perawatan suportif di ICU dan dilakukan pengeluaran zat penyebab dari tubuh serta mungkin diperlukan antidotumnya.
Jika didapat pasien tidak sadar dengan penyebab yang Belum jelas, perlu selalu difikirkan adanya kemungkinan intoksikasi. tindakan pertama:menjaga jalan nafas, oksigen ( biasanya tidak kurang dari 6 lt / menit), K/p bantuan nafas, IV line, kemudian cek seluruh tubuh adanya tanda-tanda kemungkinan mendapat obat atau racun, periksa adanya bekas suntikan, zat terminum bau nafas dan lainnya dan perkirakan juga kemungkinan terjadinya hipoglikemi.

D. Evaluasi/outcome umum pd intoksikasi
Stabilisasi & menigkatnya kardiorespirasi, kriteria :
sistolik 100mmHg, nadi 60 – 100X / menit, irama reguler
respirasi 24 X/ menit, tidak ada rales, tidak ada wheezing
meningkatnya kesadaran
1. Carbon Monoxide Poisoning
Carbon monoxide (CO), is a colorless, odorless, toxic gas that is a product of incomplete combustion. Motor vehicles, heaters, appliances that use carbon based fuels, and household fires are the main sources of this poison.
2. Carbon monoxide (CO)
Carbon monoxide (CO) intoxication is the leading cause of death due to poisoning in the United States and also the most common cause of death in combustion related inhalation injury. The incidence of non-lethal CO poisoning is not well established nor is that of unrecognized CO poisonin. Mortality rates as high as 31% have been reported in large series
3. Agent
Most immediate deaths from building fires are due to CO poisoning and therefore, fire fighters are at high risk.
a. Exogenous Sources of CO
b. Car exhaust fumes
c. Furnaces
d. Gas-powered engines
e. Home water heaters
f. Paint removers containing methylene chloride
g. Pool heaters
h. Smoke from all types of fire
i. Sterno fuel
j. Tobacco smoke
k. Wood stoves

E. Pathophysiology
In patients who die early following CO poisoning the brain is edematous, and there are diffuse petechia and hemorrhages. If the victim survives initially but dies within a few weeks, findings typical of ischemic anoxia are prominent. Interestingly, the severity of the lesions appears to correlate best with the degree of hypotension rather than with hypoxia.
1. Hypoxia and cellular asphyxia
CO combines preferentially with hemoglobin to produce COHb, displacing oxygen and reducing systemic arterial oxygen (O2) content. CO binds reversibly to hemoglobin with an affinity 200- 230 times that of oxygen. Consequently, relatively minute concentrations of the gas in the environment can result in toxic concentrations in human blood. Possible mechanisms of toxicity include: decrease in the oxygen carrying capacity of blood. Alteration of the dissociation characteristics of oxyhemoglobin, further decreasing oxygen delivery to the tissues. Decrease in cellular respiration by binding with cytochrome a3. Binding to myoglobin, potentially causing myocardial and skeletal muscle dysfunction.
2. Ischemia.
In addition to causing tissue hypoxia, CO can cause injury by impairing tissue perfusion, indicate that myocardial depression, peripheral vasodilation, and ventricular arrhythmia causing hypotension may be important in the genesis of neurologic injury.
3. Reperfusion injury
Many of the pathophysiologic changes are similar to those seen with postischemic reperfusion injuries, and similar pathology occurs in the brain in the absence of CO when hypoxic hypoxia precedes an interval of ischemia.
F. Symptomatology
Many victims of CO poisoning die or suffer permanent, severe neurological injury despite treatment. In addition, as many as 50% of those who recover consciousness and survive may experience varying degree of more subtle but still disabling neuropsychiatric sequela.
The features of acute CO poisoning are more dramatic than those resulting from chronic exposure. The clinical presentation of acute CO poisoning is variable, but in general, the severity of observed symptoms correlates roughly with the observed level of COHb:
COHb Levels and Symptomatology
a. 10% Asymptomatic or may have headaches
b. 20% Dizzyness, nausea, and syncope
c. 30% Visual disturbances
d. 40% Confusion and syncope
e. 50% Seizures and coma
f. 60% Cardiopulmonary dysfunction & death

G. Management
The mainstay of therapy for CO poisoning is supplemental O2, ventilatory support and monitoring for cardiac arrhythmias. There is general agreement that 100% oxygen should be administered prior to laboratory confirmation when CO poisoning is suspected. The goal of oxygen therapy is to improve the O2 content of the blood by maximizing the fraction dissolved in plasma (PaO2).36 Once treatment begins, O2 therapy and observation must continue long enough to prevent delayed sequelae as carboxymyoglobin unloads.
The most controversial and widely debated topic regarding CO poisoning is the use of hyperbaric oxygen (HBO). The most controversial and widely debated topic regarding CO poisoning is the use of hyperbaric oxygen (HBO) severe poisoning should be treated with 100% oxygen, with endotracheal intubation in patients who cannot protect their airway. In these patients, consideration should be given to transfusion of packed red blood cells.
H. Prognosis
30% of patients with severe poisoning have a fatal outcome.49 One study has estimated that 11% of survivors have long-term neuropsychiatric deficits, including 3% whose neurologic manifestations are delayed. One third of CO poisoning victims may have subtle but lasting memory deficits or personality changes.40. Indicators of a poor prognosis include altered consciousness at presentation, advanced age, patients with underlying cardiovascular disease, metabolic acidosis, and structural abnormalities on CT or MRI scanning.
Organophosphate and Carbamate Poisioning
Although OPC and carbamates are structurally distinct, they have similar clinical manifestations and generally the same management. Although most patients with OPC and carbamate poisoning have a good prognosis, severe poisoning is potentially lethal. Early diagnosis and initiation of treatment are important. The ED physician has access to a number of therapeutic options that can decrease morbidity and mortality.

I. Pathophysiology
OPCs and carbamates bind to 1 of the active sites of acetylcholinesterase (AChE) and inhibit the functionality of this enzyme by means of steric inhibition. The main purpose of AChE is to hydrolyze acetylcholine (ACh) to choline and acetic acid. Therefore, the inhibition of AChE causes an excess of ACh in synapses and neuromuscular junctions, resulting in muscarinic and nicotinic symptoms and signs.
Excess ACh in the synapse can lead to 3 sets of symptoms and signs. First, accumulation of ACh at postganglionic muscarinic synapses lead to parasympathetic activity of smooth muscle in lungs, the GI tract, heart, eyes, bladder, and secretory glands, and increased activity in postganglionic sympathetic receptors for sweat glands. This results in the symptoms and signs that can be remembered with the mnemonic SLUDGE/BBB. Second, excessive ACh at nicotinic motor end plates causes persistent depolarization of skeletal muscle (analogous to that of succinylcholine), resulting in fasciculations, progressive weakness, and hypotonicity. Third, as OPs cross the blood-brain barrier, they may cause seizures, respiratory depression, and CNS depression for reasons not completely understood.



J. Signs & Symptoms
Patients often present with evidence of a cholinergic toxic syndrome, or toxidrome. SLUDGE/BBB mnemonic :
S = Salivation
L = Lacrimation
U = Urination
D = Defecation
G = GI symptoms
E = Emesis
B = Bronchorrhea
B = Bronchospasm
B = Bradycardia

DUMBELS mnemonic
D = Diarrhea and diaphoresis
U = Urination
M = Miosis
B = Bronchorrhea, bronchospasm, and bradycardia
E = Emesis
L = Lacrimation
S = Salivation

K. Lab & Test
Serum cholinesterase and RBC AChE activity, which are used to estimate neuronal AChE activity. Other Tests: ECG, prolonged QTc interval is the most common ECG abnormality. Elevation of the ST segment, sinus tachycardia, sinus bradycardia, and complete heart block (rare) may also occur. (Sinus tachycardia occurs just as commonly as sinus bradycardia.)




L. Prehospital Care
Identification of the type of chemical is important. As a general rule, dimethyl OPCs undergo rapid aging, which makes early initiation of oximes critical. In comparison, diethyl compounds may cause delayed toxicity, and oxime therapy may need to be prolonged.

M. Emergency Department Care
1. ABC
Care of the ABCs should be initiated first because intubation may be necessary in cases of severe poisoning. Because succinylcholine is metabolized by means of plasma cholinesterase, OPC or carbamate poisoning may cause prolonged paralysis. Increased doses of nondepolarizing agents, such as pancuronium or vecuronium, may be required to achieve paralysis because of the excess ACh at the receptor.
Providers with appropriate personal protective equipment (PPE) can address the ABCs before decontamination atropine can precipitate ventricular fibrillation in hypoxic patients. Paradoxically, the early use of adequate atropine will dry respiratory secretions, improve muscle weakness and thereby improve oxygenation. The following should be monitored on a regular basis to assess the patient's respiratory status:
a. Respiratory rate
b. Tidal volume/ vital capacity
c. Neck muscle weakness
d. Ocular muscle involvement eg. diplopia
e. Arterial blood gas analysis
f. Cardiac monitoring, a wide range of cardiac manifestations can occur and careful haemodynamic and electrocardiac monitoring hypoxaemia, metabolic and electrolyte abnormalities can all contribute to cardiac arrhythmias. Some arrhythmias may require cardiac pacing.
2. Decontamination:
Important part of the initial care, decontamination depends on the route of poisoning. The patient's body should then be thoroughly washed with soap and water to prevent further absorption from the skin. Washing the poisioned person and removing contaminated clothes nosocomial poisoning in staff members treating patients who have been exposed to OPCs and carbamates; the odors often smelled when one cares for a patient poisoned from pesticide are commonly due to the hydrocarbon solvent, which may cause symptoms independent of the OPC agent. The patient's clothes must be removed and isolated, and his or her body washed with soap and water.GI decontamination: Oral administration of activated charcoal is a reasonable intervention after GI poisoning. Gastric emptying should then be considered if the patient presents within 1 hour of ingestion. Gastric lavage is the only means of emptying the stomach in unconscious patients in which case the airway needs to be protected.
3. Atropine
Atropine is a pure muscarinic antagonist that competes with ACh at the muscarinic receptor.
most commonly given in intravenous (IV) form at the recommended dose of 2-5 mg for adults and 0.05 mg/kg for kids with a minimum dose of 0.1 mg to prevent reflex bradycardia. Atropine may be redosed every 5-10 minutes. Severe OP poisonings often require hundreds of milligrams of atropine. In 1 case report, a patient required frequent doses of atropine and was eventually converted to an atropine infusion to a total of 30 g over 5 days.
Most sources recommend starting atropine on patients with anything more than ocular effects and then observing the drying of secretions as an endpoint in titrating to the appropriate dose. From the Tokyo sarin experience, patients poisoned by nerve agents had modest atropine requirements, with none requiring more than 10 mg. The recommended starting dose of atropine is a 2mg IV bolus. Subsequent doses of 2-5mg every 5-15 minutes should be administered until atropinization is achieved. The signs of adequate atropinization include an increased heart rate (>100 beats/min.), moderately dilated pupils, a reduction in bowel sounds, a dry mouth and a decrease in bronchial secretions.
4. Benzodiazepines
Seizures are an uncommon complication of OP poisoning. When they occur, they represent severe toxicity.
5. Other treatments
magnesium and fresh-frozen plasma as adjunctive therapy. both must be evaluated. Nebulized ipratropium bromide as an adjunct agent.



N. Management of Organophosphorus compunds poisoning
1. Skin decontamination **
2. Airway protection if indicated **
3. Gastric lavage
4. Activated charcoal 0.5-1gm/kg every 4hr
5. Anticholinesterase: Atropine/glycopyrrolate **
6. Cholinesterase reactivator: Pralidoxine
7. Ventilatory support
8. Inotropic support
9. Benzodazepines ( if seizure) **
10. Feeding-enteral/parental
** = useful

O. Further Inpatient Care
Patients who require continuous monitoring or treatment should be admitted to the ICU. Patients with clinically significant poisoning should be evaluated frequently to monitor their airway and respiratory secretions. In addition, frequent neurologic examination should be performed to evaluate for neuromuscular blockade. Therapy is largely titrated to the physical findings. Atropinization is based on the drying of respiratory secretions, and oxime therapy is based on an improvement in neuromuscular signs. A toxicologist may be of help in determining specific aging and reactivation times of the particular OPC or carbamate agent.

P. Further Outpatient Care:
Patients without any symptoms and with questionable or minimal exposure to OPs or carbamates may be considered for discharge after 6-12 hours of observation. Patients with residual neurologic symptoms should be given a follow-up appointment with a neurologist. Follow-up with a psychiatrist should be arranged as indicated.

Q. Complications
1. Intermediate syndrome, Intermediate syndrome was first described in 1987 as a sudden respiratory paresis, with weakness in cranial nerves and proximal-limb and neck flexor muscles. These clinical features appear 24-96 hours after exposure and are distinct from the previously described delayed neurotoxicity (see below). Although intermediate syndrome is incompletely understood, more recent reports suggest this is due to presynaptic and postsynaptic dysfunction of neuromuscular transmission and that it may result from insufficient oxime treatment.
2. OPC-induced delayed neurotoxicity (OPCIDN), OPCIDN is a sensorimotor polyneuropathy that typically occurs 9-14 days after OP exposure. The patient initially presents with distal motor weakness and sensory paresthesias in the lower extremities, which may progress proximally and eventually affect the upper extremities. Most sources suggest the mechanism involves inhibition of neuropathy target esterase (NTE), an enzyme that metabolizes esters in nerve cells. Some patients may recover over 12-15 months, but permanent losses with spasticity and persistent upper motor neuron findings have been reported.
3. Pancreatitis, Pancreatitis has been reported as a rare complication. One case series reported that 12.76% of OP poisonings were associated with acute pancreatitis, though this has not been the experience in other series.

R. Prognosis
In severe poisoning, death usually occurs within the first 24 hours if it is untreated. With nerve-agent poisoning, death may occur within minutes if untreated. Even with adequate respiratory support, intensive care, and specific treatment with atropine and oximes, the mortality rate is still high in severe poisonings. A delay in treatment can also lead to late and permanent neurologic sequelae. Most patients with minimal symptoms fully recover.

S. Special Concerns
Pregnant women should receive the same treatment as that given to other adults. Both atropine and pralidoxime are class C drugs in pregnancy. In the Tokyo subway attacks, 5 pregnant women were mildly poisoned, and all had normal babies without complications.