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PROBLEM 6

PROBLEM 6SHEANY LESTATILA405110062Group 3, Emergency Medicine BlockKeracunan Akibat masuknya bahan kimia tertentu ke dalam tubuh yang menyebabkan timbulnya kelainan pada tubuhJenis jenis racun : Padat : racun tikus, obat-obatan Cair : bahan peluntur, cuka getahGas : 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-lainCara 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 kesadaranPenanganan : 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, pusingPertolongan 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 darahBerikan akses IVCek kadar glukosa darah, tes darah lengkap, serum elektrolit, dan cek fungsi ginjal dan heparTatalaksana komaApabila 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 glukosaPertahankan sirkulasi kontrol sirkulasi dan tatalaksana syok dengan mengembalikan volume iv dengan infus/crystalloid sollutionTatalaksana kejangMonitor EKGLakukan bilas lambungDengan NGT/OGT dengan arang aktif (1g/kg) dicampur dengan solutio 70% sorbitolCari etiologi

2nd survey Lakukan anamnesa cepat dan tepatMengumpulkan informasi selengkap-lengkapnya untuk mengetahui penyebab Dekontaminasi etiologi penyebab toksisitasRacun yang terhirup segera pindahkan penderita dari sumber racun menuju tempat terbuka dan berikan oksigenMata yang terkontaminasiSegera bilas mata dengan air bersih atau dengan saline normalJika zat asing bersifat asam/basa dapat menggunakan pH untuk menentukan terapi

2nd survey Kulit yang terkontaminasiSegera 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 tertelanBilas 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 diriAttempted suicide Pasien memang bermaksud bunuh diriAccidental poisoning Faktor kecelakaanHomicidal poisoning Seseorang sengaja meracuni orang lainMenurut mula waktu Keracunan akutTerjadi mendadak setelah memakan sesuatu, banyak orang (makanan)Keracunan kronik Gejala perlahan & lama setelah terpajanZat penyebabnya diekresi > 24 jam, T panjang akumulasiDiagnosis Laboratorium toksikologi diagnosis pasti penyebab keracunanMembantu penegakan diagnosis:Autoanamnesis & aloanamnesisPemeriksaan fisik dugaan tempat masuknya racun inhalasi, peroral (dgn bau khas), absorbi kulit & mukosa, atau parentral berpengaruh pada efek kecepatan & lama reaksi keracunanStatus kesadaran GCSPenemuan klinis lain

Bau racunBAUPENYEBABAsetonIsopropil alkohol, asetonAlmondSinidaBawang putihArsenik, selenium, taliumTelur busukHidrogen sulfida, mekraptanWarna urinWARNAPENYEBABHijau/ biruMetilin biruKuning-merahRimfapisin, besi/ feCoklat tuaFenol, kresolButiran keputihanPrimidonCoklatMio/ haemoglobinuriaGambaran klinisKemungkinan etiologiPupil pinpoint, frek napas turunOpioid, inhibitor kolinesterase(organofosfat, carbamate insektisida), klonidin, fenotiazinDilatasi pupil, laju napas turunBenzodiazepinDilatasi pupil, takikardiaAntidepresan trisiklik, amfetamin, ekstasi, kokain, antikolinergik, antihistaminSianosisObat depresan SSP, bahan penyebab metHbHipersalivasiOrganofosfat/ karbamat, insektisidaNistagmus, ataksia, tanda serebelarAntikonvulsan(fenitoin, CMZ), alkoholGejala ekstrapiramidalFenotiazin, haloperidol, metoklopramidSeizuresAntidepresan trisiklik, antikonvulsan, teofilin, antihistamin, OAINS, fenotiazin, isoniazidHipertermiaLitium, antidepresan trisiklik, antihistaminHipertermia, hipertensi, takikardi,agitasiAmfetamin, ekstasi kokainHipertermia, takikardi, asidosis metaboliksalisilatBradikardiaBetablocker, digoksin, opioid, klonidin, antagonis kalsium(kec dihidropiridin, organofosfat insektisida)Abdominal cramp, diare, takikardi, halusinasiWithdrawal alkohol, opiat, benzodiazepinPemeriksaan Penunjang Sampel yang harus di kirim: 50ml urin, 10 ml serum, fesesPemeriksaan:Radiologi : curiga adanya aspirasi melalui inhalasi atau adanya perforasi lambungLaboratorium klinik: analisa gas darah, fungsi hati, ginjal, sedimen urin, GDSEKGPenatalaksanaan Stabilisasi (ABC)Dekontaminasi menurunkan paparan terhadap racun, mengurangi absorbsi, dan mencegah kerusakan:Dekontaminasi pulmonalDekontaminasi mataDekontaminasi kulitDekontaminasi GITEliminasi mempercepat pengeluaran racun yang sedang beredar dalam darah atau dalam saluran GIT setelah > 4jamDiuresi paksaAlkalinisasi urinAsidifikasi urinHemodialisis / peritoneal dialisisAntidotum

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

Usahakan px minum 1/> cairan berikut u/ mengencerkan racun dan menghambat penyerapannya : susu, suspense terigu,starch / kentang tumbuk yang dilumatkan dalam air, air. Rangsang px muntah : usapp dinding faring dan belakang lidah (jari/gagang sendok) tidak muntah 15 mL (1 sendok makan) sirup Ipecac1 sendok makan penuh natrium sulfat dilarutkan dalam 1,5 gelasPertahankan suhu tubuh dg meggunakan selimut. Hindari sumber panas external

Intoksikasi makanan

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23Intoksikasi MakananMakanan beracun karena :Memang mengandung zat kimia berbahaya ;ex: singkong,jamur,dsbTimbul zat beracun krn proses penyimpanan dan pemasakanTercemar oleh zat racun Dg sengaja (zat warna,penyedap,dll)MO (Stafilokokus,Salmonella,dll)Makanan mengandung ToksinEKSOTOKSIN ENTEROTOKSIN Toksin yang diproduksi & dikeluarkan oleh mikroorganisme yang masih hidupToksin yg spesifik bagi lapisan lendir usus, seperti tahan terhadap enzim tripsin & stabil terhadap panas)Makanan kaleng proses yang kurang sempurna clostridium botulinum / sporanya tumbuhMasa 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 makananMakanan mengandung ToksinEKSOTOKSIN 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 cairJika diare & muntah berat RS antimuntah & cairan IV Tindakan umum:Depresi pernapasan pernapasan buatanCegah aspirasi oaruPneumonia obat kemoterapi yang spesifikSingkong (Cassava)Patofisiologi :Singkong mengandung glikosida sianogenik linamarin (C10H17O6N) lapisan luar glukosa,aseton dan asam sianida (HCN)HCN : sianmethemoglobin, keracunan protoplasmik melumpuhkan pernafasan selMekanisme : 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

Buku Ajar Anak - IDAIManifestasi klinisTergantung jumlah kandungan HCN dalam singkongJumlah besar : kematian dalam waktu singkat akibat gagal nafasMula-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 - IDAITatalaksanaAwal Eliminasi racun muntah / bilas lambung Pemberian antidotumAmil/Na Nitrit dan Na-tiosulfatProses detoksifikasiNa-Nitrit : metHb cukup banyak mengikat NaCN tidak merusak enzim pernafasan dan sel ferisitokrom oksidase 3 % ml iv pelan-pelanNa-tiosulfat : iket NaCN terbentuk tiosianat keluar melalui paru,ludah,kencing10% iv dg dosis 0,5 ml/kgbb/kaliResusitasi dan suportifCairan IV dan Oksigenasi dengan tekanan tinggi (hiperbarik/CPAP)Buku Ajar Anak - IDAIJengkolEpidemiologi : : = 9:1Kejadian 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 makanTimbulnya gejala keracunan jengkol tergantung dari kerentanan seseorang terhadap asam jengkolat

Buku Ajar Anak - IDAIManifestasi klinisSakit pinggang, nyeri perut, muntah, sakit waktu kencingAir kemih keluar sedikit-sedikit dg butir-butir putih urin berbau jengkol dg hematuriaOliguri anuriaMuntahPegalInfiltrat pada penis,skrotum,daerah suprapubikGGA

Buku Ajar Anak - IDAITatalaksanaEliminasi racun : muntah/bilas lambungTidak ada antidotum yang khasCairan IV bila px tidak dapat minum banyakGGA : dialisis Ringan (muntah, sakit perut / pinggang saja) tidak perlu dirawat, cukup dinasehati untuk banyak minum serta memberikan Natrium bikarbonat sajaBerat (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 lainBuku Ajar Anak - IDAIBotulisme Kontaminasi o/ Clostridium botulinum dan/atau Bacteria cocovenans gliserin mjd racun toksoflavin media minyak,daging,ikan yang tidak sempurna diproses/diawetkan,makanan kalengGK/:Kelainan mata (lumpuh otot mata)Lumpuh N. Kranialis simetrisDisfagia/disartriaLumpuh otot pernapasanMuntah pada permulaan penyakit dan seringkali hebat

Talaks/:Eliminasi racun : bilas lambung,obat pencaharDepresi napas berat: pernafasan mekanis buatan Antidotum : antitoksin botulisme IV 10-50 ml setelah dilakukan tes kulitKuanidin hidroklorida lwn blokade neuromuskular dg dosis 15-35 mg/kgBB/hari dibagi dalam 3 dosisMakanan tercemar bakteriEndotoksin o/ Salmonella/Stafilokokus tumbuh dalam suhu hangat mudah dihancurkan dalam panasEx : sosis,ham,ikan,susuGK/:Muntah dan diare 3-6 jam , berlanjut 12-24 jam dan kemudian meredaKadang timbul nyeri perut hebat,demam,dehidrasi dan kaku ototTalaks/:Suportif dan simptomatis Cairan IV dan obat u/ meredam gerakan ususMakanan yang belum dimakan dipanaskan kembali slm 15 menit u/ menghancurkan toksin tsbDrugs intoxicationAcetaminophen Acute ingestion of more than 150200 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 (2436 hours)fulminant liver failure occurs hepatic encephalopathy and deathRenal failure may also occur

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Treatment antidoteacetylcysteine glutathione substitute binding the toxic metabolite as it is producedmost effective when given early and should be started within 810 hours if possibleLiver transplantation for patients with fulminant hepatic failureKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Anticholinergic Agentsinhibit 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 antidepressantUrinary retention Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Treatment Agitated patients benzodiazepine or an antipsychotic agent (eg, haloperidol)specific antidote for peripheral and central anticholinergic syndrome Physostigmine 0.51 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 asystoleCatheterization prevent excessive distention of the bladder

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007AntidepressantsTricyclic antidepressants amitriptyline, desipramine, doxepinmore than 1 g of a tricyclic (or about 1520 mg/kg) lethalManifestations tachycardia, dilated pupils, dry mouth; vasodilationCentrally mediated agitation and seizures followed by depression and hypotensionQuinidine-like cardiac toxicity wide QRS interval and depressed cardiac contractility arrythmia (ventricular conduction block and ventricular tachycardia)

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Treatment 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 50100 mEq (or 12 mEq/kg)Do not use physostigmine! aggravate depression of cardiac conduction and cause seizures

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Monoamine oxidase inhibitors tranylcypromine, phenelzineManifestations 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 seizureinteract with each other or especially with monoamine oxidase inhibitors to cause the serotonin syndromeagitation, muscle hyperactivity, and hyperthermia Bupropion seizureKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Antipsychoticsphenothiazines and butyrophenones + newer atypical drugs

Manifestations CNS depression, seizures, and hypotensionQT prolongationpotent dopamine D2 blockers parkinsonian movement disorders (dystonic reactions)neuroleptic malignant syndrome"lead-pipe" rigidity, hyperthermia, and autonomic instability

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Aspirin (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 elevatedSevere hyperthermia + Vomiting and hyperpnea fluid loss and dehydrationseizures, coma, pulmonary edema, and cardiovascular collapse

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Treatment aggressive gut decontamination gastric lavage, repeated doses of activated charcoal, whole bowel irrigationIntravenous fluids intravenous sodium bicarbonate (for moderate toxicity)emergency hemodialysis poisoning (eg, patients with severe acidosis, coma, and serum salicylate level > 100 mg/dL)

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Aspirin and other salicylat

Beta BlockersThe 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 hypertensionPropanolol Seizures and cardiac conduction block (wide QRS complex)

Treatment Glucagon is a useful antidotehigh doses (520 mg intravenously) improve heart rate and blood pressure

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Calcium Channel BlockersSmall dose toxicity depress sinus node automaticity and slow AV node conduction

ManifestationsSerious hypotension (nifedipine and related dihydropyridines)

Treatment general supportive careinitiate whole bowel irrigation + oral activated charcoal ASAPCalciumintravenously in doses of 210 g antidote for depressed cardiac contractilityglucagon, vasopressin, epinephrine & high-dose insulin+glucoseKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Carbon Monoxide & Other Toxic GasesKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007

Cholinesterase Inhibitorsorganophosphate or carbamate poisoning

Manifestations Stimulation of muscarinic receptors abdominal cramps, diarrhea, excessive salivation, sweating, urinary frequency, and increased bronchial secretionsStimulation of nicotinic receptors hypertension and either tachycardia or bradycardiaMuscle twitching and fasciculations eakness and respiratory muscle paralysisCNS effectsagitation, confusion, and seizures

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Treatment Blood testing document depressed activity of red blood cell (acetylcholinesterase) and plasma (butyrylcholinesterase) enzymesGeneral supportive care ensure that rescuers and health care providers are not poisoned by exposure to contaminated clothing or skinAntidotal treatment atropine and pralidoxime

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Cyanide 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 deathSevere metabolic acidosisvenous oxygen content may be elevated

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Treatmentrapid administration of activated charcoal + general supportive carenitrites induce methemoglobinemia, which binds to free CNthiosulfate is a cofactor in the enzymatic conversion of CNHydroxocobalamin (one form of vitamin B12) combines rapidly with CN to form cyanocobalamin

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Ethanol & Sedative-Hypnotic DrugsManifestationseuphoric and rowdy ("drunk") or in a state of stupor or coma ("dead drunk")Comatose depressed respiratory drive aspiration of gastric contentsHypothermiaEthanol blood levels greater than 300 mg/dL deep comagamma-hydroxybutyrate [GHB] overdose deeply comatose for 34 hours and then awaken fully in a matter of minutes

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Treatment General supportive care protecting the airway (including endotracheal intubation) + ventilationHypotension IV fluidbody warming if coldbenzodiazepine overdose intravenous flumazenil

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Ethylene Glycol & Methanol CNS depression and a drunken state similar to ethanol overdoseproducts of metabolism formic acid (from methanol) or hippuric, oxalic, and glycolic acids (from ethylene glycol) severe metabolic acidosis and can lead to comablindness (in the case of formic acid) renal failure (from oxalic acid and glycolic acid)

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Manifestations appears drunksevere anion gap metabolic acidosis + hyperventilationmethanol poisoning visual disturbances

Treatment fomepizole (4-methylpyrazole)inhibiting the enzyme alcohol dehydrogenaseKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Digoxin accumulation of digoxin in a patient with renal insufficiencysome patient also taking diuretics electrolyte depletion

ManifestationsVomitting Hyper- (overdose) /hypokalemia (diuretic effects) cardiac rhythm disturbances may occursinus bradycardia, AV block, atrial tachycardia with block, accelerated junctional rhythm, premature ventricular beats, bidirectional ventricular tachycardia, and other ventricular arrhythmias

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Treatment General supportive care Atropine is often effective for bradycardia or AV blockdigoxin antibodies intravenously in the dosage indicated in the package insertimprove within 3060 minutes after antibody administration

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Theophylline dose of 2030 tablets can cause serious or fatal poisoning

Manifestations sinus tachycardia and tremorVomittingHypotension, tachycardia, hypokalemia, and hyperglycemia Cardiac arrhythmias atrial tachycardias, premature ventricular contractions, and ventricular tachycardiaanticonvulsant-resistant seizureacute overdose with serum level > 100 mg/L

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Treatment General supportive care Aggressive gut decontamination repeated doses of activated charcoal and whole bowel irrigationPropanolol or other B-blocker for hypotension and tachycardiaPhenobarbital Hemodialysis serum concentrations greater than 100 mg/L and for intractable seizures in patients with lower levelsKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Intoxications managementsABCDsAirway cleared of vomitus or any other obstructionoral airway or endotracheal tube inserted if neededlateral decubitus position

Breathing assessed by observation and oximetry + arterial blood gases (if in doubt)Patients with respiratory insufficiency intubated + mechanically ventilated

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Circulation assessed by continuous monitoring of pulse rate, blood pressure, urinary output, and evaluation of peripheral perfusionintravenous line should be placedblood drawn for serum glucose and other routine determinations

Concentrated Dextrose every patient with altered mental statusunless a rapid bedside blood glucose test demonstrates that the patient is not hypoglycemicAdult 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 solutionKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007HistoryOral 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 askeddescribe the environmentsyringes, empty bottles, household productsover-the-counter medications

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Physical examinationsVital signsEyes Miosis opioids, clonidine, phenothiazines, and cholinesterase inhibitorsMydriasis amphetamines, cocaine, LSD, and atropine Horizontal nystagmus phenytoin, alcohol, barbiturates, and other sedative drugsvertical and horizontal nystagmus phencyclidine poisoningPtosis & ophthalmoplegia botulismMouth Burns corrosive substances & smoke inhalationTypical odors of alcohol, hydrocarbon solvents, or ammonia may be notedodor like bitter almonds cyanideKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Skin flushed, hot, and dry atropine and other antimuscarinicsExcessive sweating organophosphates, nicotine, and sympathomimetic drugsCyanosis hypoxemia or by methemoglobinemiaIcterus hepatic necrosis due to acetaminophen or Amanita phalloides mushroom poisoningAbdomen Ileus antimuscarinic, opioid, and sedative drugsHyperactive bowel sounds, abdominal cramping, and diarrhea organophosphates, iron, arsenic, theophylline, A phalloides, and A muscariaNervous system

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Laboratory & Imaging ProceduresArterial Blood GasesHypoventilation elevated PCO2 (hypercapnia) and a low PO2 (hypoxia)PO2 may also be low aspiration pneumonia or drug-induced pulmonary edematotal blood oxygen content or oxyhemoglobin saturation and may appear normal in patients with severe carbon monoxide poisoning

ElectrolytesSodium, potassium, chloride, and bicarbonateKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007

Renal function tests Elevated serum creatine kinase (CK) and myoglobin in the urine muscle necrosis due to seizures or muscular rigidityOxalate crystals in the urine ethylene glycol poisoning

ElectrocardiogramWidening of the QRS complex duration to more than 100 millisecondstricyclic antidepressant and quinidine overdosesQTc interval may be prolonged to more than 440 millisecondsquinidine, tricyclic antidepressants, several newer antidepressants and antipsychotics, lithium, and arsenicVariable atrioventricular (AV) block and a variety of atrial and ventricular arrhythmiasdigoxin and other cardiac glycosidesKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Toxicology Screening Teststime-consuming, expensive, and often unreliableblockers, B-blockers, and isoniazid are not included in the screening processscreening tests may be helpful in confirming a suspected intoxication or for ruling out intoxicationBUT they should not delay needed treatmentKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Decontamination Skin Contaminated clothing should be completely removeddouble-bagged to prevent illness in health care providers and for possible laboratory analysisWash contaminated skin with soap and waterKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007GI tract Emesis induced with ipecac syrupshould not be used if the suspected intoxicant is a corrosive agent, a petroleum distillate, or a rapid-acting convulsantGastric lavage patient is awake/ airway is protected by an endotracheal tube using an orogastric or nasogastric tubeLavage solutions (usually 0.9% saline) should be at body temperature

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Activated Charcoaladsorb many drugs and poisonsRatio 10:1 of charcoal to estimated dose of toxin by weightdoes not bind iron, lithium, or potassiumuseful in poisoning due to corrosive mineral acids and alkaliCatharticsWhole 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 bodiesorally at 12 L/h (500 mL/h in children) for several hours until the rectal effluent is clear

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Specific antidote Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007

Methods of Enhancing Elimination of ToxinsDialysis ProceduresPeritoneal DialysisHemodialysis enhance removal of toxic metabolites formic acid in methanol poisoningoxalic and glycolic acids in ethylene glycol poisoningespecially useful in overdose cases +precipitating drug can be removed fluid and electrolyte imbalances are present and can be corrected (salicylateintoxication)

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Forced Diuresis and Urinary pH Manipulationurinary alkalinization is useful in cases of salicylate overdoseAcidification may increase the urine concentration of drugs (phencyclidine and amphetamines)not advised worsen renal complications from rhabdomyolysis

Katzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007References Buku Ajar Ilmu Kesehatan Anak; Ikatan Dokter Anak IndonesiaKatzung BG, Masters SB, Trevor AJ, Basic Clinical Pharmacology. 11th edition. US: McGraw-Hill, 2007Pocket book of hospital care for children; WHO: 2013