PROBLEM 6SHEANY LESTATILA405110062Group 3, Emergency Medicine Block

Keracunan • Akibat masuknya bahan kimia tertentu ke dalam tubuh yang

menyebabkan timbulnya kelainan pada tubuh• Jenis – jenis racun : • Padat : racun tikus, obat-obatan • Cair : bahan peluntur, cuka getah• Gas : karbon monoksida, ammonia, nitrogen dioksida

• Sifat racun : • Korosif : merusak rongga mulut dan saluran pencernaan (asid dan

alkali)• Non korosif : obat-obatan, racun serangga, makanan tercemar

dan lain-lain• Cara racun masuk ke dalam tubuh : sentuhan kulit,

pernapasan, saluran makanan/mulut dan suntikan

Keracunan • Manifestasi klinik : pucat, muntah, sakit perut, sesak napas,

renjatan (shock), penurunan kesadaran• Penanganan : • Kenali racun • Jika pasien tidak sadarkan diri dan tidak bernafas serta tiada

denyutan nadi, lakukan CPR • Rawatan renjatan

• Tanda keracunan : • Membakar : mulut hangus/berdarah, susah bernapas, sakit,

renjatan, bibir menjadi putih • Tidak membakar : muntah, sakit perut, muka pucat, demam,

pusing

Pertolongan Segera pada Keracunan yang Mengancam Nyawa (1st survey)

• Pastikan jalan napas terbuka • Dapat diberikan tambahan oksigen, 12 L/mnt • Intubasi apabila refleks menelan (–)

• Ukur kadar gas darah arteri dan pH darah• Berikan akses IV• Cek kadar glukosa darah, tes darah lengkap, serum

elektrolit, dan cek fungsi ginjal dan hepar• Tatalaksana koma• Apabila respon pasien lemah/curiga overdosis narkotik

(pinpoint pupil, nafas lemah) naloxone 2mg setiap 1-2 mnt s/d dosis max 10-20mg

Pertolongan Segera pada Keracunan yang Mengancam Nyawa (1st survey)

• Jika diduga keracunan alkohol dan malnutrisi thiamine, 100mg IM/IV dengan kontrol glukosa

• Pertahankan sirkulasi kontrol sirkulasi dan tatalaksana syok dengan mengembalikan volume iv dengan infus/crystalloid sollution• Tatalaksana kejang• Monitor EKG• Lakukan bilas lambung• Dengan NGT/OGT dengan arang aktif (1g/kg) dicampur

dengan solutio 70% sorbitol• Cari etiologi

2nd survey

• Lakukan anamnesa cepat dan tepat• Mengumpulkan informasi selengkap-lengkapnya untuk

mengetahui penyebab• Dekontaminasi etiologi penyebab toksisitas• Racun yang terhirup segera pindahkan penderita

dari sumber racun menuju tempat terbuka dan berikan oksigen• Mata yang terkontaminasi

• Segera bilas mata dengan air bersih atau dengan saline normal• Jika zat asing bersifat asam/basa dapat menggunakan pH untuk

menentukan terapi

2nd survey

• Kulit yang terkontaminasi• Segera bilas kulit yang terkontaminasi dengan air mengalir • Pada kulit yang mengalami luka bakar dapat menggunakan kalsium

glukonat 0.5 ml dari solutio 10%

• Bilas lambung apabila diduga keracunan akibat tertelan• Bilas lambung dilakukan apabila keracunan >> dengan tanda

kesadaran menurun

Klasifikasi Menurut cara terjadinya

Self poisoning Pasien makan obat dengan dosis berlebihan tetapi dengan pengetahuan dosis ini tidak akan membahayakan, tidak bermaksud bunuh diri

Attempted suicide Pasien memang bermaksud bunuh diri

Accidental poisoning

Faktor kecelakaan

Homicidal poisoning Seseorang sengaja meracuni orang lain

Menurut mula waktu

Keracunan akut Terjadi mendadak setelah memakan sesuatu, banyak orang (makanan)

Keracunan kronik Gejala perlahan & lama setelah terpajan•Zat penyebabnya diekresi > 24 jam, T ½ panjang akumulasi

Diagnosis

• Laboratorium toksikologi diagnosis pasti penyebab keracunan• Membantu penegakan diagnosis:• Autoanamnesis & aloanamnesis• Pemeriksaan fisik dugaan tempat masuknya racun

inhalasi, peroral (dgn bau khas), absorbi kulit & mukosa, atau parentral berpengaruh pada efek kecepatan & lama reaksi keracunan• Status kesadaran GCS• Penemuan klinis lain

Bau racunBAU PENYEBABAseton Isopropil alkohol, asetonAlmond SinidaBawang putih Arsenik, selenium, taliumTelur busuk Hidrogen sulfida, mekraptan

Warna urinWARNA PENYEBABHijau/ biru Metilin biruKuning-merah Rimfapisin, besi/ feCoklat tua Fenol, kresolButiran keputihan PrimidonCoklat Mio/ haemoglobinuria

Gambaran klinis Kemungkinan etiologi

Pupil pinpoint, frek 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, antihistamin

Sianosis Obat depresan SSP, bahan penyebab metHb

Hipersalivasi Organofosfat/ karbamat, insektisida

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

Gejala ekstrapiramidal Fenotiazin, haloperidol, metoklopramid

Seizures Antidepresan trisiklik, antikonvulsan, teofilin, antihistamin, OAINS, fenotiazin, isoniazid

Hipertermia Litium, antidepresan trisiklik, antihistamin

Hipertermia, hipertensi, takikardi,agitasi Amfetamin, ekstasi kokain

Hipertermia, takikardi, asidosis metabolik salisilat

Bradikardia Betablocker, digoksin, opioid, klonidin, antagonis kalsium(kec dihidropiridin, organofosfat insektisida)

Abdominal cramp, diare, takikardi, halusinasi

Withdrawal alkohol, opiat, benzodiazepin

Pemeriksaan Penunjang

• Sampel yang harus di kirim: 50ml urin, 10 ml serum, feses• Pemeriksaan:• Radiologi : curiga adanya aspirasi melalui inhalasi atau

adanya perforasi lambung• Laboratorium klinik: analisa gas darah, fungsi hati,

ginjal, sedimen urin, GDS• EKG

Penatalaksanaan

• Stabilisasi (ABC)• Dekontaminasi menurunkan paparan terhadap racun, mengurangi

absorbsi, dan mencegah kerusakan:• Dekontaminasi pulmonal• Dekontaminasi mata• Dekontaminasi kulit• Dekontaminasi GIT

• Eliminasi mempercepat pengeluaran racun yang sedang beredar dalam darah atau dalam saluran GIT setelah > 4jam• Diuresi paksa• Alkalinisasi urin• Asidifikasi urin• Hemodialisis / peritoneal dialisis

• Antidotum

Tertelan • Bila tertelan bahan korosif(asam/basa) atau produk petroleum jangan lakukan yang no2

1. Usahakan px minum 1/> cairan berikut u/ mengencerkan racun dan menghambat penyerapannya : susu, suspense terigu,starch / kentang tumbuk yang dilumatkan dalam air, air.

2. Rangsang px muntah : usapp dinding faring dan belakang lidah (jari/gagang sendok) tidak muntah 15 mL (1 sendok makan) sirup Ipecac

3. 1 sendok makan penuh natrium sulfat dilarutkan dalam 1,5 gelas

4. Pertahankan suhu tubuh dg meggunakan selimut. Hindari sumber panas external

Intoksikasi makanan

Intoksikasi Makanan• Makanan beracun karena :

1. Memang mengandung zat kimia berbahaya ;ex: singkong,jamur,dsb

2. Timbul zat beracun krn proses penyimpanan dan pemasakan3. Tercemar oleh zat racun

1. Dg sengaja (zat warna,penyedap,dll)2. MO (Stafilokokus,Salmonella,dll)

Makanan mengandung Toksin

EKSOTOKSIN ENTEROTOKSIN Toksin yang diproduksi & dikeluarkan oleh mikroorganisme yang masih hidup

Toksin yg spesifik bagi lapisan lendir usus, seperti tahan terhadap enzim tripsin & stabil terhadap panas)

•Makanan kaleng proses yang kurang sempurna clostridium botulinum / sporanya tumbuh

•Masa inkubasi 1 – 96 jam dan gejala timbul 1 -7 hari ( tergantung penyebab)

Pencegahan: makanan kaleng dapat di masak dulu selama 15 menit

Pencemaran terjadi karena makanan dibiarkan terbuka atau spora yang masih ada tumbuh kembaliPencegahan: Makanan di simpan dalam lemari pendingin dan penderita infeksi mata & kulit sebaiknya jangan mengelola makanan

Makanan mengandung Toksin

EKSOTOKSIN ENTEROTOKSIN

•Gejala klinis (timbul 8jam – 8 hari): muntah, penglihatan ganda, kelumpuhan otot, diare dan sakit perut, ptosis dan pupil membesar, sukar menelan, lemah, kelumpuhan otot pernapasan, gangguan saluran cerna (mungkin tak terlihat)

•Gejala klinis: muntah, diare, mual, sakit perut, kejang perut, dapat demam, dehidrasi dan syok

Tindakan gawat darurat:•Usahakan muntah (beri natrium bikarbonat & karbon aktif)•Dapat dilakukan pengurasan lambung & pembersihan usus (kecuali diare)

Penanggulangan:•Muntah klorpromazin 25 – 100mg (IM/rektal)•Keracunan ringan istirahat sampai muntah berhenti (jangan di beri apa – apa melalui mulut selama 4 jam) 12-24 jam diberi makanan cair•Jika diare & muntah berat RS antimuntah & cairan IV

Tindakan umum:•Depresi pernapasan pernapasan buatan•Cegah aspirasi oaru•Pneumonia obat kemoterapi yang spesifik

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Singkong (Cassava)• Patofisiologi :• Singkong mengandung glikosida sianogenik linamarin

(C10H17O6N) lapisan luar glukosa,aseton dan asam sianida (HCN)

• HCN : sianmethemoglobin, keracunan protoplasmik melumpuhkan pernafasan sel

• Mekanisme : berikatan reversibel dengan sitokrom oksidase seluler menghambat penggunaan o2 asfiksia. Yang tidak terikat -> metabolisme tiosianat

• Uji Guinard uji singkong tersangka warna asam pikrat kuning mjd kemerahan dalam 15mnt-3 jam

• Manifestasi klinis• Tergantung jumlah kandungan HCN dalam singkong• Jumlah besar : kematian dalam waktu singkat akibat gagal nafas• Mula-mula : panas pada perut,mual,pusing,sesak,lemah nafas

cepat dg inspirasi pendek & bau bitter almond (bau nafas dan muntahan)

• Sesak disusul pingsan,kejang lemas,berkeringat,mata menonjol,pupil melebar tanpa reaksi

• Busa pada mulut tercampur warna darah dan warna kulit mjd merah bata

• Tidak ada sianosis

Buku Ajar Anak - IDAI

TatalaksanaAwal •Eliminasi racun muntah / bilas lambung

•Pemberian antidotum

Amil/Na Nitrit dan Na-tiosulfat

•Proses detoksifikasi•Na-Nitrit : metHb cukup banyak mengikat NaCN tidak merusak enzim pernafasan dan sel ferisitokrom oksidase• 3 % ml iv pelan-pelan•Na-tiosulfat : iket NaCN terbentuk tiosianat keluar melalui paru,ludah,kencing•10% iv dg dosis 0,5 ml/kgbb/kali

Resusitasi dan suportif

•Cairan IV dan Oksigenasi dengan tekanan tinggi (hiperbarik/CPAP)

Buku Ajar Anak - IDAI

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Jengkol• Epidemiologi : • ♂ : = 9:1♀• Kejadian tertinggi terdapat pada umur 4-7 tahun

• Patof : • jengkol mengandung asam jengkolat (AA yang mengandung

belerang) bertumpuknya asam jengkolat dalam tubulis distal ginjal (kristal), ureter dan uretra

• Pada anak keluhan mulai timbul 5-12 jam setelah makan• Timbulnya gejala keracunan jengkol tergantung dari kerentanan

seseorang terhadap asam jengkolat

• Manifestasi klinis• Sakit pinggang, nyeri perut, muntah, sakit waktu kencing• Air kemih keluar sedikit-sedikit dg butir-butir putih urin berbau

jengkol dg hematuria• Oliguri – anuria• Muntah• Pegal• Infiltrat pada penis,skrotum,daerah suprapubik• GGA

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• Tatalaksana• Eliminasi racun : muntah/bilas lambung• Tidak ada antidotum yang khas• Cairan IV bila px tidak dapat minum banyak• GGA : dialisis • Ringan (muntah, sakit perut / pinggang saja) tidak perlu dirawat, cukup

dinasehati untuk banyak minum serta memberikan Natrium bikarbonat saja• Berat (oliguria, hematuria, anuria dan tidak dapat minum) penderita

dirawat dan diberi infus natrium bikarbonat dalam larutan glukosa 5%. Dosis dewasa dan anak 2-5mEq/kgBB dan natrium bikarbonat diberikan secara infus selama 4-8 jam.

• Antibiotik (jika ada infeksi sekunder)

• Pencegahan : masak biji jengkol dg soda/ bikarbonat lain

Botulisme • Kontaminasi o/ Clostridium botulinum dan/atau Bacteria

cocovenans gliserin mjd racun toksoflavin media minyak,daging,ikan yang tidak sempurna diproses/diawetkan,makanan kaleng

• GK/:• Kelainan mata (lumpuh otot mata)• Lumpuh N. Kranialis simetris• Disfagia/disartria• Lumpuh otot pernapasan• Muntah pada permulaan penyakit dan seringkali hebat

• Talaks/:• Eliminasi racun : bilas lambung,obat pencahar• Depresi napas berat: pernafasan mekanis buatan • Antidotum : antitoksin botulisme IV 10-50 ml setelah dilakukan

tes kulit• Kuanidin hidroklorida lwn blokade neuromuskular dg dosis 15-

35 mg/kgBB/hari dibagi dalam 3 dosis

Makanan tercemar bakteri• Endotoksin o/ Salmonella/Stafilokokus tumbuh dalam suhu

hangat mudah dihancurkan dalam panas• Ex : sosis,ham,ikan,susu• GK/:• Muntah dan diare 3-6 jam , berlanjut 12-24 jam dan kemudian

mereda• Kadang timbul nyeri perut hebat,demam,dehidrasi dan kaku otot

• Talaks/:• Suportif dan simptomatis Cairan IV dan obat u/ meredam

gerakan usus• Makanan yang belum dimakan dipanaskan kembali slm 15

menit u/ menghancurkan toksin tsb

Drugs’ intoxication

Acetaminophen • Acute ingestion of more than 150–200 mg/kg (children) or 7 g

total (adults)• highly toxic metabolite is produced in the liver

• Manifestations • Asymptomatic, mild gastrointestinal upset (nausea, vomiting)• elevated aminotransferase levels and hypoprothrombinemia (24–

36 hours)• fulminant liver failure occurs hepatic encephalopathy and

death• Renal failure may also occur Ka

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• Treatment • antidote acetylcysteine

• glutathione substitute binding the toxic metabolite as it is produced

• most effective when given early and should be started within 8–10 hours if possible

• Liver transplantation for patients with fulminant hepatic failure

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Anticholinergic Agents• inhibit the effects of acetylcholine at muscarinic receptors

• Manifestations• "red as a beet" (skin flushed)• "hot as a hare" (hyperthermia)• "dry as a bone" (dry mucous membranes, no sweating)• "blind as a bat" (blurred vision, cycloplegia)• "mad as a hatter" (confusion, delirium)• Muscle twitching • seizures are unusual

• unless the patient has ingested an antihistamine or a tricyclic antidepressant

• Urinary retention

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• Treatment • Agitated patients benzodiazepine or an antipsychotic agent (eg,

haloperidol)• specific antidote for peripheral and central anticholinergic

syndrome • Physostigmine 0.5–1 mg IV + monitoring (bradycardia and seizures)• should not be given to a patient with suspected tricyclic

antidepressant overdose aggravate cardiotoxicity, resulting in heart block or asystole

• Catheterization prevent excessive distention of the bladder

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Antidepressants• Tricyclic antidepressants

• amitriptyline, desipramine, doxepin• more than 1 g of a tricyclic (or about 15–20 mg/kg) lethal• Manifestations

• tachycardia, dilated pupils, dry mouth; vasodilation• Centrally mediated agitation and seizures followed by depression

and hypotension• Quinidine-like cardiac toxicity wide QRS interval and depressed

cardiac contractility arrythmia (ventricular conduction block and ventricular tachycardia)

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• Treatment • Endotracheal intubation and assisted ventilation • Intravenous fluids are given for hypotension + dopamine/NE (if

necessary)• antidote for quinidine-like cardiac toxicity (manifested by a wide QRS

complex) sodium bicarbonate; bolus of 50–100 mEq (or 1–2 mEq/kg)

• Do not use physostigmine!• aggravate depression of cardiac conduction and cause seizures

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• Monoamine oxidase inhibitors • tranylcypromine, phenelzine

• Manifestations • severe hypertensive reactions when interacting foods or drugs are

taken • interact with the selective serotonin reuptake inhibitors (SSRIs)

• Newer antidepressants • fluoxetine, paroxetine, citalopram, venlafaxine (SSRIs) can cause

seizure• interact with each other or especially with monoamine oxidase

inhibitors to cause the serotonin syndrome• agitation, muscle hyperactivity, and hyperthermia

• Bupropion seizure

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Antipsychotics• phenothiazines and butyrophenones + newer atypical drugs

• Manifestations • CNS depression, seizures, and hypotension• QT prolongation• potent dopamine D2 blockers

• parkinsonian movement disorders (dystonic reactions)• neuroleptic malignant syndrome• "lead-pipe" rigidity, hyperthermia, and autonomic instability

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Aspirin (Salicylate)• Acute ingestion of more than 200 mg/kg • chronic overmedication

uncoupling of oxidative phosphorylation and disruption of normal cellular metabolism

• Manifestations • hyperventilation and respiratory alkalosis • Metabolic acidosis follows, an increased anion gap • Body temperature may be elevated• Severe hyperthermia + Vomiting and hyperpnea fluid loss and

dehydration• seizures, coma, pulmonary edema, and cardiovascular collapse

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• Treatment • aggressive gut decontamination

• gastric lavage, repeated doses of activated charcoal, whole bowel irrigation

• Intravenous fluids • intravenous sodium bicarbonate (for moderate toxicity)• emergency hemodialysis

• poisoning (eg, patients with severe acidosis, coma, and serum salicylate level > 100 mg/dL)

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Aspirin and other salicylat

Beta Blockers• The most toxic blocker is propranolol• At high doses it may cause sodium channel blocking effects similar to

those seen with quinidine-like drugs + lipophilic (enter the CNS)

• Manifestations • Bradycardia and hypotension • Agents with partial agonist activity (eg, pindolol) tachycardia and

hypertension• Propanolol Seizures and cardiac conduction block (wide QRS complex)

• Treatment • Glucagon is a useful antidote

• high doses (5–20 mg intravenously) improve heart rate and blood pressure

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Calcium Channel Blockers• Small dose toxicity • depress sinus node automaticity and slow AV node conduction

• Manifestations• Serious hypotension (nifedipine and related dihydropyridines)

• Treatment • general supportive care• initiate whole bowel irrigation + oral activated charcoal ASAP• Calcium

• intravenously in doses of 2–10 g antidote for depressed cardiac contractility

• glucagon, vasopressin, epinephrine & high-dose insulin+glucose

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Carbon Monoxide & Other Toxic Gases

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Cholinesterase Inhibitors• organophosphate or carbamate poisoning

• Manifestations • Stimulation of muscarinic receptors

• abdominal cramps, diarrhea, excessive salivation, sweating, urinary frequency, and increased bronchial secretions

• Stimulation of nicotinic receptors • hypertension and either tachycardia or bradycardia

• Muscle twitching and fasciculations eakness and respiratory muscle paralysis

• CNS effects• agitation, confusion, and seizures

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• Treatment • Blood testing

• document depressed activity of red blood cell (acetylcholinesterase) and plasma (butyrylcholinesterase) enzymes

• General supportive care • ensure that rescuers and health care providers are not poisoned

by exposure to contaminated clothing or skin• Antidotal treatment

• atropine and pralidoxime

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Cyanide • binds readily to cytochrome oxidase inhibiting oxygen

utilization within the cell cellular hypoxia and lactic acidosis

• Manifestations • shortness of breath, agitation, and tachycardia followed by

seizures, coma, hypotension, and death• Severe metabolic acidosis• venous oxygen content may be elevated

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• Treatment• rapid administration of activated charcoal + general supportive

care• nitrites induce methemoglobinemia, which binds to free CN–

• thiosulfate is a cofactor in the enzymatic conversion of CN–

• Hydroxocobalamin (one form of vitamin B12) combines rapidly with CN– to form cyanocobalamin

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Ethanol & Sedative-Hypnotic Drugs• Manifestations• euphoric and rowdy ("drunk") or in a state of stupor or coma

("dead drunk")• Comatose depressed respiratory drive aspiration of gastric

contents• Hypothermia• Ethanol blood levels greater than 300 mg/dL deep coma• gamma-hydroxybutyrate [GHB] overdose deeply comatose for

3–4 hours and then awaken fully in a matter of minutes

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• Treatment • General supportive care • protecting the airway (including endotracheal intubation) +

ventilation• Hypotension IV fluid• body warming if cold• benzodiazepine overdose intravenous flumazenil

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Ethylene Glycol & Methanol• CNS depression and a drunken state similar to ethanol

overdose• products of metabolism formic acid (from methanol) or

hippuric, oxalic, and glycolic acids (from ethylene glycol)• severe metabolic acidosis and can lead to coma• blindness (in the case of formic acid) • renal failure (from oxalic acid and glycolic acid)

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• Manifestations • appears drunk• severe anion gap metabolic acidosis + hyperventilation• methanol poisoning visual disturbances

• Treatment • fomepizole (4-methylpyrazole)

• inhibiting the enzyme alcohol dehydrogenase

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Digoxin• accumulation of digoxin in a patient with renal insufficiency• some patient also taking diuretics electrolyte depletion

• Manifestations• Vomitting • Hyper- (overdose) /hypokalemia (diuretic effects)• cardiac rhythm disturbances may occur

• sinus bradycardia, AV block, atrial tachycardia with block, accelerated junctional rhythm, premature ventricular beats, bidirectional ventricular tachycardia, and other ventricular arrhythmias

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• Treatment • General supportive care • Atropine is often effective for bradycardia or AV block• digoxin antibodies

• intravenously in the dosage indicated in the package insert• improve within 30–60 minutes after antibody administration

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Theophylline • dose of 20–30 tablets can cause serious or fatal poisoning

• Manifestations • sinus tachycardia and tremor• Vomitting• Hypotension, tachycardia, hypokalemia, and hyperglycemia • Cardiac arrhythmias

• atrial tachycardias, premature ventricular contractions, and ventricular tachycardia

• anticonvulsant-resistant seizure• acute overdose with serum level > 100 mg/L Ka

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• Treatment • General supportive care • Aggressive gut decontamination

• repeated doses of activated charcoal and whole bowel irrigation• Propanolol or other B-blocker for hypotension and tachycardia• Phenobarbital • Hemodialysis

• serum concentrations greater than 100 mg/L and for intractable seizures in patients with lower levels

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Intoxication’s managements

ABCDs• Airway • cleared of vomitus or any other obstruction• oral airway or endotracheal tube inserted if needed• lateral decubitus position

• Breathing • assessed by observation and oximetry + arterial blood gases (if in

doubt)• Patients with respiratory insufficiency intubated + mechanically

ventilated

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• Circulation • assessed by continuous monitoring of pulse rate, blood pressure,

urinary output, and evaluation of peripheral perfusion• intravenous line should be placed• blood drawn for serum glucose and other routine determinations

• Concentrated Dextrose • every patient with altered mental status

• unless a rapid bedside blood glucose test demonstrates that the patient is not hypoglycemic

• Adult 25 g (50 mL of 50% dextrose solution) intravenously • Children 0.5 g/kg (2 mL/kg of 25% dextrose)• Alcoholic or malnourished

• 100 mg of thiamine intramuscularly or in the intravenous infusion solution

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History• Oral statements about the amount and even the type of drug

ingested in toxic emergencies may be unreliable

• family members, police, and fire department or paramedical personnel should be asked• describe the environment• syringes, empty bottles, household products• over-the-counter medications

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Physical examinations• Vital signs• Eyes • Miosis opioids, clonidine, phenothiazines, and cholinesterase

inhibitors• Mydriasis amphetamines, cocaine, LSD, and atropine • Horizontal nystagmus phenytoin, alcohol, barbiturates, and other

sedative drugs• vertical and horizontal nystagmus phencyclidine poisoning• Ptosis & ophthalmoplegia botulism

• Mouth • Burns corrosive substances & smoke inhalation• Typical odors of alcohol, hydrocarbon solvents, or ammonia may be

noted• odor like bitter almonds cyanide

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• Skin • flushed, hot, and dry atropine and other antimuscarinics• Excessive sweating organophosphates, nicotine, and

sympathomimetic drugs• Cyanosis hypoxemia or by methemoglobinemia• Icterus hepatic necrosis due to acetaminophen or Amanita

phalloides mushroom poisoning• Abdomen • Ileus antimuscarinic, opioid, and sedative drugs• Hyperactive bowel sounds, abdominal cramping, and diarrhea

organophosphates, iron, arsenic, theophylline, A phalloides, and A muscaria

• Nervous system

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Laboratory & Imaging Procedures• Arterial Blood Gases• Hypoventilation elevated PCO2 (hypercapnia) and a low PO2

(hypoxia)• PO2 may also be low aspiration pneumonia or drug-induced

pulmonary edema• total blood oxygen content or oxyhemoglobin saturation and may

appear normal in patients with severe carbon monoxide poisoning

• Electrolytes• Sodium, potassium, chloride, and bicarbonate

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• Renal function tests • Elevated serum creatine kinase (CK) and myoglobin in the urine

muscle necrosis due to seizures or muscular rigidity• Oxalate crystals in the urine ethylene glycol poisoning

• Electrocardiogram• Widening of the QRS complex duration to more than 100 milliseconds

• tricyclic antidepressant and quinidine overdoses• QTc interval may be prolonged to more than 440 milliseconds

• quinidine, tricyclic antidepressants, several newer antidepressants and antipsychotics, lithium, and arsenic

• Variable atrioventricular (AV) block and a variety of atrial and ventricular arrhythmias• digoxin and other cardiac glycosides

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Toxicology Screening Tests• time-consuming, expensive, and often unreliable• blockers, B-blockers, and isoniazid are not included in the

screening process• screening tests may be helpful in confirming a suspected

intoxication or for ruling out intoxication• BUT they should not delay needed treatment

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Decontamination • Skin • Contaminated clothing should be completely removed• double-bagged to prevent illness in health care providers and for

possible laboratory analysis• Wash contaminated skin with soap and water

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• GI tract • Emesis

• induced with ipecac syrup• should not be used if the suspected intoxicant is a corrosive agent, a

petroleum distillate, or a rapid-acting convulsant• Gastric lavage

• patient is awake/ airway is protected by an endotracheal tube using an orogastric or nasogastric tube

• Lavage solutions (usually 0.9% saline) should be at body temperature

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• Activated Charcoal• adsorb many drugs and poisons• Ratio 10:1 of charcoal to estimated dose of toxin by weight• does not bind iron, lithium, or potassium• useful in poisoning due to corrosive mineral acids and alkali

• Cathartics• Whole bowel irrigation with a balanced polyethylene glycol-

electrolyte solution (GoLYTELY, CoLyte) after ingestion of iron tablets, enteric-coated medicines, illicit drug-filled packets, and foreign bodies

• orally at 1–2 L/h (500 mL/h in children) for several hours until the rectal effluent is clear Ka

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Specific antidote

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Methods of Enhancing Elimination of Toxins• Dialysis Procedures• Peritoneal Dialysis• Hemodialysis

• enhance removal of toxic metabolites • formic acid in methanol poisoning• oxalic and glycolic acids in ethylene glycol poisoning

• especially useful in overdose cases +• precipitating drug can be removed • fluid and electrolyte imbalances are present and can be corrected

(salicylate intoxication)

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• Forced Diuresis and Urinary pH Manipulation• urinary alkalinization is useful in cases of salicylate overdose• Acidification may increase the urine concentration of drugs

(phencyclidine and amphetamines)• not advised worsen renal complications from rhabdomyolysis

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References • Buku Ajar Ilmu Kesehatan Anak; Ikatan Dokter Anak Indonesia• Katzung BG, Masters SB, Trevor AJ, Basic Clinical

Pharmacology. 11th edition. US: McGraw-Hill, 2007• Pocket book of hospital care for children; WHO: 2013