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Kamis, 07 Oktober 2010

Gadar (Gawat Darurat)

KEPERAWATAN GAWAT DARURAT (KEGAWAT DARURATAN & KEKRITISAN) :

FILOSOFI, KONSEP HOLISTIK & PROSES KEPERAWATAN
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 professional
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
a. Pasien dr segala umur dng diagnosa, tidak terdiagnosa atau maldiagnosis problem dng
kompleksitas yg bervariasi.
b. 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 )
a. KARAKTERISTIK UNIK PRAKTEK KEP. GADAR
• Pengkajian, diagnosa, terai baik yg urgen / non urgen individual dari berbagai umur pasien
walaupun dng data / informasi yg sangat terbatas
• Triage & Prioritas
• Persiapan bencana alam
• Stabilisasi & resusitasi
• Krisis intervensi u/ populasi ps yg UNIk spt korban kekerasan sexual
• Pemberian perawatan pd lingkungan yg tidak terkontrol atau yg tidak dpt diprrediksikan

b. KERANGKA KERJA PROSES KEP. EN

• TUJUAN
• Menyelamatkan hidup
• PENGKAJIAN
Pada sistem yg terganggu
U/ memperbaiki kegagalan atau mempertahankan sistem
• DIAGNOSIS
Mencari perbedaan u/ menemukan tanda-tanda & gejala
• PERENCANAAN
Berdasarkan protokol dan prosedur
• INTERVENSI
Terapi ditujukan pd penanganan gejala krisis & stabilisasi ps.
Diteruskan s/d pasien stabil u/ dpt pindah atau ditransportasikan ke unit lain atau meninggal
• EVALUASI
Dilakukan scr cepat u/ menilai keefektifan
KEGAWATAN OBSTETRIK
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. Diagnostic Peritoneal Lavage (DPL)
)Diagnostic Peritoneal Lavage (DPL) A. Purpose of DPL 1. Trauma a. Intraabdominal
hemorrhage b. Visceral injury c. Perforation 2. Other indications a. Pancreatitis b. Peritonitis c.
Strangulating bowel d. Intestinal obstruction e. Malignant cells in peritoneal washing B. Case :
“The doctor says I want to do a DPL on this patient. . . What do you need??” 1. Arrow DPL kit
(found in each trauma room) 2. Sterile gloves, gown, box of 4x4 gauze, pkg of sterile towels 3.
Cleaning agent- Povidone iodine or chlorhexidine 4. Warmed 0.9% saline solution or Ringer’s
lactate (physicians choice) 5. Patient labels, requisitions and specimen tubes a. no. 11 blade and
(1) no. 15 blade 6. 1% or 2% lidocaine with epinephrine C. Preparation and Set-up 1. Obtain
appropriate consent 2. Ensure that the child’s stomach and bladder are decompressed 3. If needed
place orogastric (OG) or nasogatric (NG) tube to decompress the stomach and a foley to drain
the bladder 4. This will avoid puncturing the bladder or bowel. 5. Place child on a full monitor to
record vital signs during procedure. 6. Assemble appropriate supplies 7. Establish sterile field 8.
Perform “Time-Out” 9. Assist MD by setting up lavage equipment 10. This ensures that the
warm fluid is available as soon as catheter is placed and that a closed system is quickly
established. 11. Assist with the administration of lidocaine 12. MD performs the initial tap to
access the peritoneal space and to assess abdominal pathology. 13. Initial aspirate is drawn,
labeled appropriately and sent to the lab. 14. If the tap is dry (no fluid was obtained) a small
incision may be made at the linea alba. This will facilitate catheter insertion. 15. After insertion
of the catheter IV tubing and fluid are attached. Fluid can be instilled with a syringe or by
gravity. 16. 10-20ml/kg to a max of 1L. 17. The fluid is used to rinse the peritoneal cavity. 18.
Fluid is drained out of the peritoneal cavity by placing the IV fluid bag in a dependent position
19. After all fluid has been removed the MD will remove the catheter and suture the incision 20.
Remove ~20cc fluid from the return, place in specimen tubes and send to lab for analysis D.
How do I know if my DPL is positive?? 1. Grossly bloody fluid 2. Red blood cell (RBC) count
greater than 100,000/mm3. The threshold may be smaller for a child with penetrating trauma to
the abdomen or chest. 3. White blood cell (WBC) count greater than 500/mm3. 4. Presence of
bacteria, bile, stool or amylase in the abdominal fluid. E. If your DPL is positive. . . 1. Prepare
the child 2. for the Operating Room 3. A positive DPL indicates intraabdominal injury that
requires surgical intervention. INTOKSIKASI 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.
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