Dasar-dasar Penatalaksanaan Keracunan.2013

KULIAH BLOCK 21: EMERGENCY MEDICINE AND TRAUMATOLOGY

Disampaikan oleh :Anggoro Budi Hartopo

Bagian Kardiologi dan Kedokteran VaskularBagian Ilmu Penyakit Dalam

Fakultas Kedokteran Universitas Gadjah Mada

DASAR-DASAR DASAR-DASAR PENATALAKSANAAN PENATALAKSANAAN

KERACUNANKERACUNAN

DASAR-DASAR DASAR-DASAR PENATALAKSANAAN PENATALAKSANAAN

KERACUNANKERACUNAN

Oleh :Rizka HumardewayantiRizka Humardewayanti

Siti NurdjanahSiti Nurdjanah

Diagnosis : Anamnesis Pemeriksaan Fisik, tanda-tanda

umum : Keracunan akut Kesadaran Pernafasan Tanda-tanda vital

Lab. Rutin & toksikologi

Penurunan KesadaranPenurunan Kesadaran

Tingkat I Mengantuk, tapi mudah diajak bicara

Tingkat II Sopor, dapat dibangunkan dengan rangsangan

minimal : bicara keras, lengan digoyangkan Tingkat III

Sporo-komatus bereaksi dengan rangsangan maksimal : menggosokkan kepalan tangan

Tingkat IV Koma tak bereaksi sama sekali prognosis

jelek

Pernafasan Depresi pusat pernafasan, air-way

perhatikan Tekanan darah

Penurunan tekanan darah shok : dehidrasi, gangguan pusat vasomotor

Kejang-kejang Rangsangan pada SSP

Pupil & refleks Diameter pupil & reflek otot rangka tak

penting untuk diagnosis Bising usus

Penurunan kesadaran TK III : biasanya (-)TK IV : selalu (-)

Tanda-tanda lainTanda-tanda lain

Gangguan : Irama jantung Asam basa, elektrolit Kerusakan organ Gastrointestinal dll

Tabel. Karakteristik Warna Urin

Warna urin Penyebab

Hijau / biruKuning-merahCoklat tuaButiran keputihanCoklat

Metilin biruRifampisin, besi (Fe)Fenol, kresolPrimidonMio/haemoglobinuria

Tabel : Gambaran Klinis yang dapat menunjukkan Bahan penyebab keracunan

Gambaran klinis Kemungkinan penyebab

Pupil pin point, frekuensi napas turun Opioid, inhibitor kolinesterase (organofosfat, carbamate insektisida), Klonidin, Fenotiazin.

Dilatasi pupil, laju napas, turun Benzodiazepin

Dilatasi pupil, takikardia Antidepresan trisiklik, Amfetamin, ekstasi, kokain, Antikolinergik (benzeksol, benztropin), Antihistamin

Sianosis Obat depresan SSP, bahan penyebab methaemoglobinemia.

Hiper saliva Organofosfat / karbamat, insekstisida

Nistagmus, ataksia, tanda serebelar Antikonvulsan (fenitoin, karbamazepin), alkohol

Gejala ekstrapiramidal Fenotiazin, haloperidol, metoklopramid,

Seizures Antidepresan trisiklik, antikonvulsan, teofilin, antihistamin, OAINS, fenothiazin, Isoniazid.

Hiperthermia Litium, antidepresan trisiklik, antihistamin.

Hiperthermia & hipertensi, takikardi, agitasi

Amfetamin, ekstasi, kokain.

Hiperthermia & takikardi, asidosis metabolik.

Salisilat

Bradikardia Penghambat beta, digoksin, opioid, klonidin, antagonis kalsium (kecuali dihidropiridin) Organofosfat insekstisida.

Abdominal cramp, diare, takikardi, halusinasi

Withdrawal alkohol, opiat, benzodiazepin

TERAPI SUPORTIF Bebaskan jalan nafas Oksigenasi/ventilasi Terapi aritmia Perbaiki hemodinamik Hilangkan kejang Koreksi abnormalitas suhu Koreksi kelainan metabolik Hindari komplikasi sekunder

Pencegahan Terhadap Pencegahan Terhadap Absorbsi Racun Lebih LanjutAbsorbsi Racun Lebih Lanjut

Dekontaminasi Gastrointestinal Syrup ipecac untuk menginduksi muntah Bilas lambung Arang aktif Irigasi usus Pencahar Dilusi Pengeluaran melalui endoskopi atau

tindakan bedah

Dekontaminasi permukaan lain Dekontaminasi mata Dekontaminasi kulit Evakuasi racun dari rongga-rongga

tubuh

Mempercepat Eliminasi Mempercepat Eliminasi RacunRacun Multiple dose arang aktif Diuresis paksa Mengubah pH urin Chelasi Pengeluaran extracorporal

Dialisis peritoneal - Hemofiltrasi Hemodialisis - Plasmapherin Hemoperfusi - Transfusi

tukar Oxigen Hiperbarik

Penggunaan AntidotumPenggunaan Antidotum Netralisasi dengan antibodi Netralisasi dengan bahan kimia Antagonis metabolik Antagonis fisiologis

Hindari Pemaparan Ulang Pengarahan bagi orang dewasa Jauhkan dari jangkauan anak-anak Membaca cara penggunaan Rujukan Psikiatri

Terapi SuportifTerapi Suportif (1) (1)

A. Bebaskan jalan nafas Tidur terlentang, kepala ekstensi,

miring (bila mutah) Mulut bersihkan Pasang guedel Bila mungkin ET

B. Oksigenasi / ventilasi Tanpa alat pernafasan :

Mulut mulut Mulut hidung

Alat bantu pernafasan : Alat penghubung Balon masker Ventilator automatik Mesin pernafasan automatik


C. Terapi aritmia akibat hipoksia/ketidak seimbangan elektrolit cari causa

Bradikardia jangan segera obati, mungkin kompensasi

Akibat : hipotensi, syncope : Atropin 0.01 – 0.03 mg/Kg BB I.V. Tak berhasil : isoproterenol 1-10

mcg/menit I.V. titrasi sampai normal


Takikardia Bila tak berhubungan hipotensi/nyeri

dada observasi + obat sedatif Symptomatik induced takikardia :

prpranolol 0.01 – 0.03 mg/kg i.v. Anticholinergik induced takikardia :

physostigmine 0.01 – 0.03 mg/kg iv/neostigmin 0.01 – 0.03 mg/kg i.v.


Hemodinamik Hipotensi 200 ml Nacl i.v

bolus/kristaloid isotonik lain 1-2 lt tak respon : dopamin 5-15 mg/dog/net per infus

Akibat overdosis anti depresan : sodium bicarbonat 1-2 meq /kg injeksi

Hipertensi Phentolamin 2-5 mg iv/ Sodium nitroprused 0.25 – 8ug/kg/mt iv Bila + takikardi propranolol 1-5 mg iv


D. Terapi kejang Hati-hati antikonvulsan hipotensi

cardial arrest, respiratory arrest Bila digunakan terlalu cepat

Diazepam 0.1-0.2 mg/kg iv Phenobarbitol 0.1-0.2 mg/kg iv bila

iv sulit


E. Koreksi Suhu Hipotermia selimut/cairan hangat iv,

hangatkan udara pernafasan Hipertermia tanggalkan pakaian, semprot air

suam kuku, kipasi penderita

F. Koreksi Gangguan Metabolik Sesuai sebab yang mendasari

G. Cegah komplikasi sekunder Berdasar jenis racun & reaksi yang akan timbul


Mencegah absorbsi racun lebih Mencegah absorbsi racun lebih lanjutlanjut

Dekontaminasi GIT1. Induksi muntah syrup ipecal tak

efektif setelah pemberian arang aktif K.I. :

penderita mengantuk Asam /alkali bun toksik perforasi Kerosen aspirasi Kejang

15 cc ipecal ½ gelas air 30’ emesis ulangAnak-anak 10 cc Bila tak mutah bilas lambung

2. Bilas lambung Indikasi :

< 1 jam Penderita dengan histeri/koma jalan

udara dilindungi Kontraindikasi :

Tertelan asam basa Minyak tanah Kejang Kelebihan cairan meningkatkan

absorbsi racun

Tehnik bilas lambung: Beri air 1 gelas Posisi Trendelenburg Ukur panjang pipa dari mulut lambung

tandai Gigi palsu /benda asing dimulut keluarkan Buka mulut penahan Masukkan pipa Aspirasi toksikologi 100-300 cc air hangat (37oC) dari 3 lt bilas

terakhir : 50 gr arang aktif Koma Endotracheal Tube

3. Arang aktif Suspensi + air / pecahan botol

sus/sedotan/pipa NGT kecil 1-2 g/kg BB + 8 cc air; bisa +

pemanis /perasa Bilas racun tertelan dalam lumen

usus charcoal-toxin-complex.

4. Irigasi usus Pipa gastrik 0.5 lt/jam (anak)

2 lt/jam (dewasa) Posisi duduk Cairan pembersih usus : t.d.

elektrolit & polyethileneglikol

5. Pencahar Sorbitol 1-2 g/kg BB Mg Sulfat 30 gr

6. Dilusi/pengenceranMinum 5 ml/kg BB air/cairan jernih secepat

mungkin setelah minum toksin

7. Pengeluaran endoskopi/bedahJarang digunakan. Keracunan logam bera

lethal arsenic, besi, mercury, thalium

8. Dekontaminasi permukaan cairAir , NaCl fisiologis

Mempercepat eliminasi racun

Dosis multiple arang aktif 1 gr /kg BB setiap 2-4 jam

Diuresis paksa/mengubah pH urin Alkaline – diuresis Saline – diuresis Acid – diuresis Tak digunakan lagi

Pengeluaran racun secara extracorporal

Syarat dialisis : Berat molekul rendah Kelarutan tinggi Protein – binding rendah Volume distribusi kecil Half-life panjang

Indikasi : Penderita dg penurunan kesadaran cepat Kadar toksin darah lethal Gangguan detoksifikasi alami : gagal hati, ginjal

Penanganan beberapa bahan toksin

Gejala :Depresi pernafasan MiosisHipotensi BradikardiHipotermi Edema pulmonarBising usus menurun HiporefleksiKejang

Overdosis Opiat (morphin, pethidin, heroin, kodein)

Penanganan overdosis opiat

Tindakan penanganan kegawatan Bebaskan jalan nafas Berikan oksigen 100% sesuai

kebutuhan Pasang infus - Dextrosa 5% atau NaCL 0,9%, - Cairan koloid bila diperlukan

Pemberian antidotum naloxone (1) Tanpa hipoventilasi : dosis awal diberikan

0,4 mg iv. Dengan hipoventilasi : dosis awal diberikan

1-2 mg iv. Bila tidak ada respon dalam 5 menit,

diberikan nalokson 1-2 mg iv hingga timbul respon perbaikan kesadaran dan hilangnya depresi pernafasan, dilatasi pupil atau telah mencapai dosis maksimal 10 mg.

Pemberian antidotum naloxone (2) Efek nalokson berkurang 20-40 menit dan

pasien dapat jatuh kedalam keadaan overdosis kembali, sehingga perlu pemantauan ketat tanda-tanda penurunan kesadaran, pernafasan dan perubahan pada pupil serta tanda vital lainnya selama 24 jam. Untuk pencegahan dapat diberikan drip nalokson 1 ampul dalam 500 cc D5% atau NaCL 0,9% diberikan dalam 4-6 jam.

Suportif Simpan sampel urin untuk pemeriksaan opiat

urin dan lakukan foto thoraks Pertimbangkan pemasangan ETT

(endotracheal tube) bila : Pernafasan tidak adekuat Oksigenasi kurang meski ventilasi cukup Hipoventilasi menetap setelah pemberian

nalokson ke-2 Pasien dipuasakan untuk menghindari

aspirasi akibat spasme pilorik.

Gambar: Alur tatalaksana intoksikasi opium

Intoksikasi golongan opiat

AloanamnesaRiwayat pemakaian obat

Bekas suntikan (needle track sign)Pemeriksaan urin

Trias intoksikasi opiatDepresi napasPupil pin-point

Kesadaran menurun (koma)

Support sistem pernapasan dan sirkuslasi

Nalokson intravena (lihat protokol)

Observasi/pengawasan tanda vital danDipuasakan selama 6 jam

Gambar :Protokol penanganan intoksikasi opiat di Unit Gawat Darurat

Pasien pengguna obat

Emergensi Tidak emergensi

REHABILITASI

Detoksifikasi konvensional di RS/berobat jalan Detoksifikasi cepat dengan anestesi

PulangHCUICU

Ruang rawat inap

Observasi 6 jam rawat

Tidak Ya

Indikasi rawat

IGD

Tidak ya

Indikasi rawat

Poliklinik Jalan

OverdosisGejala putus obat/kegawatan psikiatri

Emergensi komplikasi (ARDS, AIDS, dll)

Masalah psikiatriMasalah komunikasi

(HCV, pneumonia, drug abuse, HIV, dll)

Penanganan sesuai besar masalahPenanganan sesuai besar masalah

Perburukan

Poliklinik Rawat jalan

Berobat lanjut(kontrol rutin)

Ruang rawatInap Penyakit dalampsikiatri

Keracunan Bisa Kalajengking

Gejala lokal Nyeri seperti terbakar Gejala peradangan + parestesi lokal p.u. membaik beberapa jam

Gejala sistemik Gelisah Hiperhidrosis Diplopia Nistagmus Fasikulasi

Salivasi Hipertensi Takikardi Kejang Paralisis otot

pernafasan

Edema paru Syok Koagulopati koagulasi intra vaskuler

diseminata Pankreatitis Fugsi ginjal menurun Hb uria Ikterus Hipertermia asidosis

Penatalaksanaan Stabilasi ABC Dekontaminasi

Cuci luka Bila perlu ATS 1200/unit

Terapi spesifik Beri antivenin serum skorpion (polivalue)

Peringatan Jangan lakukan

insisi lokal/pengisapan ! Kompres es

Terapi lain sesuai perjalanan penyakit

Gigitan Ular / Snake byte

Faktor yang mempengaruhi keparahan : Usia, kesehatan pasien Lokasi gigitan Bisa ular Sekunder infeksi Gerakan pasien

Penanganan gigitan ular : Ditenangkan memperlambat

penyerapan Pembebatan sampai aliran limfe,

pembuluh darah jangan terkena Segera ke RS Antiveni

ABO dosis tergantung efek dan bisa ular ke pasien. Bisa diulang tipa 2 jam

Gejala gigitan ular berbisa (1) Gejala lokal

Edema Nyeri tekan Ekimosis (30 mnt – 24 jam)

Gejala sistemik: Hipotensi Kelemahan otot Berkeringat Gigil Mual, hipersalivasi, mutah Nyeri kepala

Gejala hematotoksik : perdarahan Gejala neurotoksik :

Hipertonik Paresis lisis otot/pernafasan Kejang – koma

Kardiotoksik Sindrom kompartemen : edema tungkai

dengan tanda-tanda : 5p (pain, pallor, parestesia, paralisis,

pulselesmess

Gejala gigitan ular berbisa (2)

Penatalaksanaan Menghalangi/memperlambat

absorbsi bisa ular Menetralkan bisa ular Mengatasi efek lokal & sistemik

Tindakan Sebelum ke pusat pengobatan :

Mobilisasi Jangan manipulasi gigitan Tindakan mengikat (< 30 menis

pasca gigitan) bag. Proksimal gigitan menahan aliran limfe / bukan untuk vena atau arteri

Di Pusat Pengobatan ABC Beri SABU (serum anti bisa ular), 2 vial 5 ml

+ 500 ml Nacl 0.9% per drip (i.v.) atau dextrose 5% 40 – 80 tts/mnt. Maksimal 100 ml (20 vial)

Pedoman terapi SABU mengacu pada Schwartz dan Way (Depkes, 2001). Derajat 0 & 1 evaluasi 12 jam, SABU tak perlu Derajat II 3 – 4 vial SABU Derajat III 5 – 15 vial SABU Derajat IV : berikan penambahan 6 – 8 vial SABU

Klasifikasi gigitan ular menurut Schwartz

Derajat

Venerasi

Luka Nyeri Edema/eritema sistemik

0 0 + +/- < 3 cm/12 jam 0

I +/- + + 3 – 12 cm/12 jam 0

II + + +++ >12 – 25 cm/12 jam+, neurotoksik, mual, pusing, syok

II + + +++ >25 cm/12 jam++, ptechiae, syok, ekhimosis

IV +++ + +++ >ekstremitas++, GGA, koma, perdarahan

Tambahan terapi :- Sesuai efek samping lainnya- ATS profilaksis- AB spektrum luas

Carbon Monoxide (CO) An odorless, colorless, tasteless gas Results from incomplete combustion of

carbon-containing fuels Gasoline, wood, coal, natural gas, propane,

oil, and methane CO is the #1 cause of poisoning in

industrialized countries

KERACUNAN CARBONMONOKSIDA

Pathophysiology CO displaces O2 from hemoglobin binding sites CO prevents O2 from binding (carboxyhemoglobin) COHb increases O2 affinity, interfering with normal

release

Half-life of Carbon Monoxide Half-life – time required for half the

quantity of a drug or other substance to be metabolized or eliminated

CO half-life on 21% room air O2 – 4 - 6 hours

CO half-life on 100% O2 – 80 minutes CO half-life with hyperbaric O2 – 22

minutes

CO Poisoning: The Great Imitator

30-50 % of CO-exposed patients presenting to Emergency Departments are misdiagnosed

Barker MD, et al. J Pediatr. 1988;1:233-43

Barret L, et al. Clin Toxicol. 1985;23:309-13

Grace TW, et al. JAMA. 1981;246:1698-700

Severity of Intoxication:Morbidity Associated with COHb and Duration

Highlighted Area demonstrates current OSHA Standard for CO:

[500ppm/30 minutes]

Consider 500 ppm/60-90 minutes….

Signs and Symptoms

SpCO%

Clinical Manifestations

<5% None

5-10% Mild headache, tire easily

11-20%

Moderate headache, exertional SOB

21-30%

Throbbing headache, mild nausea, dizziness, fatigue, slightly impaired judgment

31-40%

Severe headache, vomiting, vertigo, altered judgment

41-50%

Confusion, syncope, tachycardia

51-60%

Seizures, unconsciousness

Carbon Monoxide Poisoning Presents Like the Flu!

Increased Risks

Health and activity levels can increase the risk of signs and symptoms at lower concentrations of CO

Infants Women who are pregnant

Fetus at greatest risk because fetal hemoglobin has a greater affinity for oxygen and CO compared to adult hemoglobin

Elderly Physical conditions that limit the body’s ability to use oxygen

Emphysema, asthma Heart disease

Physical conditions with decreased O2 carrying capacity Anemia – iron-deficiency & sickle cell

CO Identification Sooner the suspicion the

sooner the appropriate treatment can be initiated

CO Assessment

1. Every patient, every time.

2. All occupants at CO alarm calls.

3. Firefighters.

CDC Diagnostic Criteria Suspected CO exposure

Potentially exposed person but no credible threat exists

Probable CO exposure Clinically compatible case where credible

threat exists Confirmed CO exposure

Clinically compatible case where biological tests have confirmed exposure

Management of CO poisoning Oxygen 100 % ASAP ABG COHb ECG CXR Cardiac enzymes Cardiac monitoring

Clinical evaluation Maintain a high level of suspicion History of exposure can be absent COHb

< 3 % non-smokers or < 10 % in smokers not predictive of outcome correlation with symptoms useless

ABG : metabolic acidosis ( lactate ) ECG : ischemia, arrythmias

Neurologic evaluation

Neurologic examination Mental status examination

Folstein Psychometric testing

CO Neuropsychological Screening Battery Neuroradiologic imaging : CT, MRI

Carbon Monoxide Levels Venous sampling > 10% abnormal Levels correlate poorly with

severity of exposurre

Pulse CO-oximeter Device

Hand-held device Attaches to a finger tip similar to pulse ox

device Most commonly measured gases in commercial

devices include Carbon monoxide (SpCO) Oxygen (SpO2) Methemoglobin (SpMet) Other combustible gases

Without the device, need to draw a venous sample of blood to test for CO levels

Treatment CO Poisoning

Increasing the concentration of inhaled oxygen can help minimize the binding of CO to hemoglobin

Some CO may be displaced from hemoglobin when the patient increases their inhaled oxygen concentrations

Treatment begins with high index of suspicion and removal to a safer environment

Immediately begin 100% O2 delivery

Treatment

High-flow, FiO2 ~100%, normobaric O2 O2 shortens the half life of COHb

21% O2 = 4-6 hours 100% O2 = 40-80 minutes 100% O2 2.5atm = 15-30 minutes

Continue O2 until COHb normal Beware concomitant smoke inhalation and burn

injury Normobaric v Hyperbaric O2 therapy

HBO hastens resolution of acute symptoms Unclear evidence for effect of HBO on late

complications and mortality

Triage & Treatment Algorithm

CO Triage and Treatment Algorithm

Measure COHb% (SpCO)

0 – 5% > 5%

No further medical evaluation of SpCO

needed.

SpCO > 15or

SpO2 < 90

SpCO < 15and

SpO2 > 90

100% oxygen & transport to ED

Symptoms of CO &/or Hypoxia

Yes No

100% oxygen & transport to ED

No further treatment of SpCO required Give out CO Info Sheet recommending a. Nonsmokers should evaluate home/ work environment for CO b. Smokers should consider tobacco cessation treatment.NOTE:

If Cardiac Symptoms, add MI ProtocolIf Asthma Symptoms, add Albuterol

Hyperbaric Oxygen Decrease COHb

half life Displaces CO

from tissues Improves oxygen

carrying capacity Limits lipid

peroxidation Improves

dissolved oxygen

Hyperbaric Oxygen: Indications

Neurological damage Cardiovascular events Loss of Consciousness Persistent symptoms COHb > 25% ( some centers use >40%) COHb > 15% in pregnant woman Ideally within 6 hours of exposure

Adverse effects of HBO

Need for transfer to HBO facility with risk of deterioration

Otic barotrauma effusion, hemorrahge, TM rupture

CNS oxygen toxicity : seizures Epistaxis

Prevention of CO poisoning Public education about CO poisoning Identification of activities at risk Training of workers for proper use of

propane-powered tools Appropriate ventilation of confined places Industrial and domestic use of CO detectors Reporting to public health services

Prognosis

Difficult to predict the long-term effects of CO poisoning/exposure. Even with proper medical treatment a few

people can develop long-term brain damage.

Some individuals appear to have no long-term affects.

If pregnant, fetal complications or death may result.

Initial management of coma

A Airway control

B Breathing

C Circulation

D Drugs (give all three) :Dextrose 50%, 50-100 mL IVThiamine, 100 mg IM or IVNaloxone, 0,45-2 mg IV1

And consider flumazenil, 0,2-0,5 mg IV2

1Repeated doses, up to 5-10 mg, may be required.2Do not give if patient has coingested a tricyclic antidepressant or other convulsant drug or has a seizure disorder.

Convulsions related to toxins or drugs requiring special

consideration.

Toxin or Drug Comment

Isoniazid (INH) Administer pyridoxine

Lithium May indicate need for hemodialysys.

Organophosphates Administer pralidoxime (2-PAM) and atropine

StrychnineConvulsions are actually spinally mediated muscle spasms and usually require neuromuscular paralysis

TheophyllineConvulsions indicate need for hemodialysis or charcoal hemoperfusion

Tricyclic antidepressant

Hyperthermia and cardiotoxicity are common complicationss of repeated convulsions; paralyze early with neuromuscular blockers to reduce muscular hyperactivity

Some toxic agents for which there are specific antidotes

Toxic Agent Specific Antidote

Acetaminophen Acetylcysteine

Anticholinergics (eg, atropine) Physostigmine

Anticholinesterases (eg, organophosphate pesticides)

Atropine and pralidoxime (2-PAM)

Benzodiazepines Flumazenil

Carbon monoxide Oxygen

Cyanide Sodium nitrite, sodium thiosulfate

Digitalis glycosides Digoxin-Specific fab antibodies

Heavy metals (eg, lead, mercury, iron) and arsenic

Specific chelating agents

Isoniazid Pyridoxine (vitamin B6)

Methanol, ethylene glycol Ethanol (ethyl alcohol)Or fomepizole (4-methylprazole)

Opoids Naloxone, nalmefene

Snake venom Specific antivenin

Recommended use of hemodialysis (HD) and hemoperfusion (HP) in poisoning

Poison Procedure1 indications2

Carbamazepine HP Seizures, severe cardiotoxicity

Ethylene glycol HD Acidosis, serum level > 50 mg/dl

Lithium HDSevere symptoms; level >4 meq/L more than 12 hours after last dose

Methanol HD Acidosis, serum level >50 mg/dl

Phenobarbital HPIntractable hypertension, acidosis despite maximal supportive care

Salicylate HDSevere acidosis, CNS symptoms, level > 100 mg/dl (acute overdose) or >60 mg/dl (chronic intoxication)

Theophylline HP or HDSerum level >90-100 mg/L (acute) or seizures and serum level >40-60 mg/L (chronic)

Valproic acid HDSerum level > 900-1000 mg?L or deep coma, severe acidosis

1Contac a regional poison control center or a clinical toxicologist before undertaking these procedure

Example of common drugs screened for in blood and urine in a reference toxicology laboratory

BloodAcetaminophenAlcoholsBarbituratesBenzodiazepinesCarbamazepineCarisoprolol

EthchlorvynolGlutethimideMeprobamidePhenytoinSalicylates

UrineAcetaminophenAlcoholsAmphetaminesBarbituratesChlorpheniramineCocaineCodeineDextromethorphanDiphenhydraminelidocaine

MepperidineMeprobamateMethadoneMorphinePentazocinePhencyclidinePhenothiazinesPropoxypheneSalicylatesTricyclic antidepressants

Examples of common drugs screened in blood and urine in a reference toxicology laboratory

Drug or Toxin Treatment

Acetaminophen Specific antidote (acetylcysteine) based on serum level

Carbon monoxide

High carboxythemoglobin level indicates need for 100% oxygen, consideration of hyperbaric oxygen

Carbamazepine High level may indicate need for hemoperfusion or hemodialysis

Digoxin On basis of serum digoxin level and severity of clinical presentasion, treatment with Fab antibody fragments (Digibind) may be indicated.

Ethanol Low serum level may suggest nonalcoholic cause of coma (eg, trauma, other drugs, other alcohols). Serum ethanol may also be useful in monitorring ethanol therapy for metathol or ethylene glycol poisoning.

Iron Level may indicate need for chelation with deferoxamine

Lithium Serum levels can guide decision to institute hemodialysis

Methanol, ethylene glycol

Acidosis, high levels indicate need for hemodialysis, therapy with ethanol or fomepizole.

Methemoglobin Methemoglobinemia can be treated with methylene blue intravenously.

Salicylates High level may indicate need for hemodialysis, alkaline diuresis

Theophylline Immediate hemodialysis or hemoperfusion may be indicated based on serum level

Valproic acid Elevated levels may indicate need to consider hemodialysis.

Common corrosive agents

Category and Examples Injury Caused

Concentrated alkaliesClinitest tabletsDrain cleanersIndustrial-strength ammoniaLyeOven cleaners

Penetrating liquefactionNecrosis

Concentrate acidsPool disinfectantsToilet bowl cleaners

Coagulation necrosis

Weaker clening agentsCationic detergents (diswaher detergents)Household ammoniaHousehold bleach

Superficial burns and irritation; deep burns (rare)

OtherHydrofluoric acid

Penetration, delayed, destructive injury

Contoh Intoksikasi di Rumah tangga

Detergen & Pembersih Sabun Bahan pemutih Pembersih lantai/porselin Yang mengandung amonia

Gejala : Sabun iritasi ringan kulit, mata, G.E. Nausea, vomitus, diare Peradangan mukosa nyeri perut Mutah darah Berak hitam Berat perforasi

Terapi Diberi minum segera untuk pengenceran Rangsang mutah/bilas lambung KI

Bahan Alkali

Pembersih kamar mandi kaustik mengandung carbonat, hidroksida atau fosfat

Gejala : Rasa terbakar pada mulut & dada Disfagia afagia refluks bila min/mak Mutah darah Berat syok Bila sembuh striktur esofagus

Terapi : Beri air/susu untuk membersihkan alkali Pemberian asam untuk menetralisisr tidak

direkomendasikan Rangsang mutah / bilas lambung KI

Bahan asam Gejala :

Rasa terbakar pada mulut, dada, perut Eritematous bibir & sekitar mulut Disfagia, mutah darah Suara usus Perforasi Striktur esofagus stenosis

Terapi : Rangsang mutah/bilas lambung KI Minum air banyak menetralisir Monitor adanya perforasi usus

Alkohol Etil alkohol Isopropil alkohol Metil alkohol

Etil alkohol Minuman :

Wiski 40 – 50% Anggur 10 – 15% Bir 2 – 8%

Gejala : Nausea, vomitus Depresi Inkoordinasi, ataksia, hipotermia

Terapi : 2 jam post minum rangsang mutah, bilas lambung Bila sudah ada tanda-tanda depresi SSP absorbsi

sudah terjadi, tindakan diatas sia-sia. Koreksi keseimbangan cairan basa asam, elektrolit

Dekstrose 50%

Isopropil Alkohol Sebagai desinfektan, cairan penyegar kulit

(sebagai campuran) hair tonic, dll Efek :

Depresi SSP 3 kali > potent daripada ethanol Absorbsi melalui G6, TR Resp.

Gejala : Nausea Vomitus Bingung Stupor koma Hipotermia Hipotensi

Terapi : Rangsang mutah Bilas lambung

Metil Alkohol Cairan pembersih Cutex Methanol / miras Gejala :

Nausea Vomitus Nyeri abdomen Depresi SSP medriasis kebutaan mata

Terapi : Rangsang mutah Bilas lambung Beri ethanol kompetitif inhibitor dengan methanol Sodium bicarbonat koreksi asidosis metabolik

Dasar-dasar Penatalaksanaan Keracunan.2013

Documents