preskas igd intoksikasi carbamate

5/24/2018 PRESKAS IGD Intoksikasi Carbamate

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Carbamate Intoxication

Mira Puspita


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DATA DASAR

Nama : Ny. A

Usia : 23 tahun

Tanggal MRS: 29 April 2014 pukul 23.50 WITA

KU :

Tidak sadar setelah minum obat serangga


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PRIMARY SURVEY

A : Gargling

B : Spontan, RR 42x/menit, SaO280%

C : Nadi 128x/menit, akral dingin, merah,

basah, CRT 3

D : Unresponsive, pupil:pinpoint

GDS : 219 mg/dl


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TATALAKSANA AWAL

Pasien masuk P1/critical care

O2masker Jackson Rees10 lpm

Dekontaminasi

Suction

Pasang monitor

Pasang IV lineguyur 1000cc

Intubasi (atracurium 50mg + diazepam 10mg )

Pasang NGT, Kateter urin,

Cek DL, Ur/Cr, OT/PT, GDS


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SECONDARY SURVEY

RPS :

Pasien ditemukan keluarga dalam keadaan lemas 6jam SMRS. Kepada keluarga os mengatakan telah

meminum obat pembunuh hama satu tutup botolkecil. Lalu 5 jam SMRS pasien dibawa ke puskesmasAlas. Lalu dr PKM di rujuk ke RSUD Sumbawa, dalamperjalanan pasien tidak sadarkan diri.

Menurut keluarga obat pembunuh hama ygdiminum oleh pasien adalah Sidabas


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RPD :

Riwayat HT (-), DM (-), riw. Sakit Jantung (-), Riw.

Stroke, trauma, koma, kejang, operasi disangkal

Riw. Keluarga

HT (-), DM (-)


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Pemeriksaan Fisik

KU : Tampak sakit berat, terpasang ETT,TD 157/90 mmHg, Nadi

138x/mnt reguler dan kuat, RR 38x/mnt,suhu 360C

Kepala : deformitas (-), nyeri tekan (-),

Mata : konjungtiva pucat -/- , sklera ikterik -/- ,pupil miosis +/+ 1 mm, lakrimasi(+)

Mulut : Hipersalivasi (+) Leher : Pembesaran KGB (-), tiroid dbn, JVP flat


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Jantung : S1-S2 reguler, murmur (-), gallop (-)

Paru : Vesikuler +/+, wheezing -/-, rhonki -/-, broncore +/+

Abdomen : supel, datar, shifting dullness (-),turgor normal, Hati

dan Limpa tidak membesar, BU (+)

Ekstremitas : Akral dingin, CRT 3, sianosis (-)

Secondary Survey


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TATALAKSANA LANJUTAN

Lanjut guyur RL 500 cc

Atropin 1 gr (4 ampul)


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Irama : Sinus TakikardiLaju : 137x/mnt

Axis : Normoaxis

Gel.P : Durasi 0,08 s, tinggi 1 mm

Pmitral (-), P pulmonal (-)

Interval PR : 0,12 s

Gel.Q : Q patologis (-)


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Komplex QRS :

Durasi komplex QRS 0,12 s

R V5 + S V1 < 35 kk

Segmen ST : isoelektrik, ST depresi (-), ST elevasi (-)

Gel. T : T inverted (-)

Interval QT :Gel. U : negatif


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Kesan : irama sinus takikardi, normoaxis, tidakada hipertrofi ventrikel kanan maupun kiri,

tidak terdapat gangguan iskemik


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Hasil Laboratorium

KESAN : LEUKOSITOSIS


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Rontgen Thorax

Kesan :

Tampak

perselubungan pada

kedua lapang paru ec

bronchorea dd

aspirasi


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KESAN :

ASIDOSIS RESPIRATORIK

BLOOD GAS ANALYSIS


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WORKING DIAGNOSIS

Intoksikasi Carbamate


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Tatalaksana

Inf. RL 30 tpm

Inj. Ceftriaxone 2 gr

Inj. Ranitidin I amp

Inj. Ondancentron 8 mg

Inj. Atropin 1 gr setiap 10-15 menit sampai

terdapat tanda atropinisasi Rawat ICU


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FOLLOW UP ICU 30/4/2014 S : Tidak sadar

O :

Terpasang ETT

TTV :

TD : 140/90 mmHg

N : 100x/m

RR 12 ( terpasang ventilator)

Sat O2 99%

Pf :

mata : pupil isokor 2mm/2mm Thorax : SJ I-II reguler, murmur (-), gallop (-), SN vesikuler +/+, bronkore minimal +/+

Ekstremitas : akral hangat

A : Intoksikasi Carbamate

P :

IVFD RL : D5 : aminofusin = 1:1:1

Inj. Ceftriaxon 2 x 1 gr

Sulfas atropin 4x1 amp

Metilprednisolon 3 x 125 mg

Ranitidin 2 x 50 mg

Piracetam 3x 3 gr

Citicolin 2 x 250 mg Midazolam 2,5 m k


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TINJAUAN PUSTAKA

INSECTICIDES INTOXICATION


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Pesticide Intoxication

Pesticides include insecticides, herbicides, androdenticides

Insecticides are :

Organophosphates

Carbamates

Organochlorines

Pyrethin/pyrethroids

Neonicotinoids

N1N-diethyl-3-methylbenzamide (DEET)


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Organophosphates

Diazinon, acephate, malathion, parathion

Inhibit enzyme acethylcholinesterase

Extremely well absorbed from the lungs, GItract, skin, mucous membranes, and

conjunctiva following inhalation, ingestion, or

topical contact.


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Carbamates

N-methyl carbamates (carbaryl, pirimicarb,

propoxur, trimethacarb) are cholinesterase

inhibitors that are structurally related to the

organophosphate compounds.

Medicinal forms include physostigmine,

pyridostigmine, and neostigmine

Carbamates can be toxic after dermal,

inhalation, and GI exposure


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ASETILKOLIN

KOLINASAMASETAT

ASETILKOLINESTERASE


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TREATMENT IN EMERGENCY ROOM

ABC

Decontamination

Atropine

Atropine is most commonly given in intravenous(IV) form at the recommended dose of 2-5 mg foradults and 0.05 mg/kg for kids with a minimumdose of 0.1 mg to prevent reflex bradycardia.

Atropine may be redosed every 5-10 minutes.Severe OP poisonings often require hundreds ofmilligrams of atropine.


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TERIMA KASIH


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OPCs and carbamates bind to an active site of acetylcholinesterase (AChE) and inhibit thefunctionality of this enzyme by means of steric inhibition. The main purpose of AChE is to hydrolyzeacetylcholine (ACh) to choline and acetic acid. Therefore, the inhibition of AChE causes an excess ofACh in synapses and neuromuscular junctions, resulting in muscarinic and nicotinic symptoms andsigns.

Excess ACh in the synapse can lead to 3 sets of symptoms and signs.

First, accumulation of ACh at postganglionic muscarinic synapses leads to parasympathetic activityof smooth muscle in the lungs, GI tract, heart, eyes, bladder, and secretory glands and increased

activity in postganglionic sympathetic receptors for sweat glands. This results in the symptoms andsigns that can be remembered with the mnemonic SLUDGE/BBB (see Physical below). Second,excessive ACh at nicotinic motor end plates causes persistent depolarization of skeletal muscle(analogous to that of succinylcholine), resulting in fasciculations, progressive weakness, andhypotonicity. Third, as OPs cross the blood-brain barrier, they may cause seizures, respiratorydepression, and CNS depression for reasons not completely understood.

OPCs and carbamates also bind to erythrocyte cholinesterase (also known as RBC cholinesterase)on RBCs and plasma cholinesterase (also known as pseudocholinesterase, serum cholinesterase, or

butyrylcholinesterase) in the serum. This binding seems to have only minimal clinical effects but isuseful in confirmatory diagnostic studies.

The main difference in the mechanisms of action between OPCs and carbamates is that carbamatesspontaneously hydrolyze from the AChE site within 24 hours, whereas OPCs undergo aging. Agingoccurs when the phosphorylated AChE nonenzymatically loses an alkyl side chain, becomingirreversibly inactivated. Carbamates, however, reversibly bind to the active site and do not undergoaging.


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Carbamates can be toxic after dermal, inhalation, and GIexposure. Carbamates transiently and reversibly bind toand inhibit the cholinesterase enzyme throughcarbamylation. This occurs by transiently binding to aserine hydroxyl residue at the active site of the

cholinesterase enzyme. Regeneration of enzyme activity bydissociation of the carbamyl-cholinesterase bond occurswithin minutes to a few hours involving rapid, spontaneoushydrolysis of the carbamate-cholinesterase bond.Therefore, aging does not occur. A major difference from

organophosphate poisoning is that new enzyme does notneed to be synthesized before normal function is restoredafter carbamate poisoning


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In adults, symptoms of acute carbamate

poisoning are similar to the cholinergic crisisobserved with organophosphate agents but are

of shorter duration.Because carbamates do noteffectively penetrate the central nervous systemin adults, less central toxicity is seen, and seizuresdo not occur. However, in children, presentation

of carbamate poisoning differs, with apredominance of central nervous systemdepression and nicotinic effects.14


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Initial treatment of carbamate poisoning is the same as fororganophosphorus compounds. Atropine is the antidote of choice and isadministered for muscarinic symptoms. This is usually all that is necessarywhile waiting for the carbamylated acetylcholinesterase complex todissociate spontaneously and recover function, usually within 24 hours.Therapy usually is not needed for more than 6 to 12 hours. The use of

pralidoxime in carbamate poisoning is controversial.3335

The carbamate-binding half-life to cholinesterase is approximately 30 minutes, andirreversible binding does not occur; therefore, there is little need forpralidoxime. Human case reports and some but not all animal studiessuggest that pralidoxime may potentiate the toxicity ofmonomethylcarbamate, such as carbaryl.34As such, pralidoxime should beavoided in known single-agent carbaryl poisonings. However, pralidoxime

should be used in mixed poisonings with an organophosphorus compoundand a carbamate or if the type of insecticide is unknown.


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Senyawa organophospat adalah

senyawa kimia yang mengandung

ikatan carbon-phospat

Carbamates adalah senyawa kimia

organik yang tersusun atas asam

carbamic


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Menghambat kolinesterase

Orghanophospat > phosphorylasi

Carbamates > carbamilasi

Orghanophospat menimbulkan aging (terjadi

ikatan ireversibel orghanophospat-kolinesterse)

Terjadi Kolinergik Exsess

preskas igd intoksikasi carbamate

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