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 (Materi Dasar Keperawatan)
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 yang 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 (Materi Dasar Keperawatan)

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 ( Materi Dasar Keperawatan)

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.

Mata Kuliah KMB 1 S1 Keperawatan

Patofisiologi ablatio retina

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