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
Terapi SuportifTerapi Suportif (2) (2)
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
Terapi SuportifTerapi Suportif (3) (3)
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.
Terapi SuportifTerapi Suportif (4) (4)
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
Terapi SuportifTerapi Suportif (5) (5)
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
Terapi SuportifTerapi Suportif (6) (6)
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
Terapi SuportifTerapi Suportif (7) (7)
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
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
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
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