Carbamate Intoxication

Mira Puspita
DATA DASAR
Nama : Ny. A
Usia : 23 tahun
Tanggal MRS: 29 April 2014 pukul 23.50 WITA

KU :
Tidak sadar setelah minum obat serangga
PRIMARY SURVEY
A : Gargling
B : Spontan, RR 42x/menit, SaO
2
80%

C : Nadi 128x/menit, akral dingin, merah,
basah, CRT 3
D : Unresponsive, pupil:pinpoint
GDS : 219 mg/dl
TATALAKSANA AWAL
Pasien masuk P1/critical care
O
2
masker Jackson Rees 10 lpm
Dekontaminasi
Suction
Pasang monitor
Pasang IV line guyur 1000cc
Intubasi (atracurium 50mg + diazepam 10mg )
Pasang NGT, Kateter urin,
Cek DL, Ur/Cr, OT/PT, GDS

SECONDARY SURVEY
RPS :
Pasien ditemukan keluarga dalam keadaan lemas 6
jam SMRS. Kepada keluarga os mengatakan telah
meminum obat pembunuh hama satu tutup botol
kecil. Lalu 5 jam SMRS pasien dibawa ke puskesmas
Alas. Lalu dr PKM di rujuk ke RSUD Sumbawa, dalam
perjalanan pasien tidak sadarkan diri.

Menurut keluarga obat pembunuh hama yg
diminum oleh pasien adalah Sidabas
RPD :
Riwayat HT (-), DM (-), riw. Sakit Jantung (-), Riw.
Stroke, trauma, koma, kejang, operasi disangkal
Riw. Keluarga
HT (-), DM (-)

Pemeriksaan Fisik
KU : Tampak sakit berat, terpasang ETT,
TD 157/90 mmHg, Nadi
138x/mnt reguler dan kuat, RR 38x/mnt,
suhu 36
0
C
Kepala : deformitas (-), nyeri tekan (-),
Mata : konjungtiva pucat -/- , sklera ikterik -/- ,
pupil miosis +/+ 1 mm, lakrimasi(+)
Mulut : Hipersalivasi (+)
Leher : Pembesaran KGB (-), tiroid dbn, JVP flat

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

TATALAKSANA LANJUTAN
Lanjut guyur RL 500 cc
Atropin 1 gr (4 ampul)

Irama : Sinus Takikardi
Laju : 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 (-)


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





Kesan : irama sinus takikardi, normoaxis, tidak
ada hipertrofi ventrikel kanan maupun kiri,
tidak terdapat gangguan iskemik

Hasil Laboratorium
KESAN : LEUKOSITOSIS
Rontgen Thorax
Kesan :
Tampak
perselubungan pada
kedua lapang paru ec
bronchorea dd
aspirasi
KESAN :
ASIDOSIS RESPIRATORIK
BLOOD GAS ANALYSIS
WORKING DIAGNOSIS
Intoksikasi Carbamate



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
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 mg kp

TINJAUAN PUSTAKA

INSECTICIDES INTOXICATION
Pesticide Intoxication
Pesticides include insecticides, herbicides, and
rodenticides
Insecticides are :
Organophosphates
Carbamates
Organochlorines
Pyrethin/pyrethroids
Neonicotinoids
N1N-diethyl-3-methylbenzamide (DEET)
Organophosphates
Diazinon, acephate, malathion, parathion
Inhibit enzyme acethylcholinesterase
Extremely well absorbed from the lungs, GI
tract, skin, mucous membranes, and
conjunctiva following inhalation, ingestion, or
topical contact.
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
ASETILKOLIN
KOLIN
ASAM
ASETAT
ASETILKOLINES
TERASE


ORGANOFOSPAT
Ireversible
Fosforilasi
Menembus
Blood Brain
Barrier
Seizures (+)
KARBAMAT
Reversible
Karbamilasi
Tidak
menembus
Blood Brain
Barrier
Seizures (-)
TREATMENT IN EMERGENCY ROOM
ABC
Decontamination
Atropine
Atropine is most commonly given in intravenous
(IV) form at the recommended dose of 2-5 mg for
adults and 0.05 mg/kg for kids with a minimum
dose of 0.1 mg to prevent reflex bradycardia.
Atropine may be redosed every 5-10 minutes.
Severe OP poisonings often require hundreds of
milligrams of atropine.
TERIMA KASIH
OPCs and carbamates bind to an active site of acetylcholinesterase (AChE) and inhibit the
functionality of this enzyme by means of steric inhibition. The main purpose of AChE is to hydrolyze
acetylcholine (ACh) to choline and acetic acid. Therefore, the inhibition of AChE causes an excess of
ACh in synapses and neuromuscular junctions, resulting in muscarinic and nicotinic symptoms and
signs.
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 activity
of 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 and
signs 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, and
hypotonicity. Third, as OPs cross the blood-brain barrier, they may cause seizures, respiratory
depression, 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 is
useful in confirmatory diagnostic studies.
The main difference in the mechanisms of action between OPCs and carbamates is that carbamates
spontaneously hydrolyze from the AChE site within 24 hours, whereas OPCs undergo aging. Aging
occurs when the phosphorylated AChE nonenzymatically loses an alkyl side chain, becoming
irreversibly inactivated. Carbamates, however, reversibly bind to the active site and do not undergo
aging.

Carbamates can be toxic after dermal, inhalation, and GI
exposure. Carbamates transiently and reversibly bind to
and inhibit the cholinesterase enzyme through
carbamylation. This occurs by transiently binding to a
serine hydroxyl residue at the active site of the
cholinesterase enzyme. Regeneration of enzyme activity by
dissociation of the carbamyl-cholinesterase bond occurs
within minutes to a few hours involving rapid, spontaneous
hydrolysis of the carbamate-cholinesterase bond.
Therefore, aging does not occur. A major difference from
organophosphate poisoning is that new enzyme does not
need to be synthesized before normal function is restored
after carbamate poisoning
In adults, symptoms of acute carbamate
poisoning are similar to the cholinergic crisis
observed with organophosphate agents but are
of shorter duration. Because carbamates do not
effectively penetrate the central nervous system
in adults, less central toxicity is seen, and seizures
do not occur. However, in children, presentation
of carbamate poisoning differs, with a
predominance of central nervous system
depression and nicotinic effects.
14


Initial treatment of carbamate poisoning is the same as for
organophosphorus compounds. Atropine is the antidote of choice and is
administered for muscarinic symptoms. This is usually all that is necessary
while waiting for the carbamylated acetylcholinesterase complex to
dissociate 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, and
irreversible binding does not occur; therefore, there is little need for
pralidoxime. Human case reports and some but not all animal studies
suggest that pralidoxime may potentiate the toxicity of
monomethylcarbamate, such as carbaryl.
34
As such, pralidoxime should be
avoided in known single-agent carbaryl poisonings. However, pralidoxime
should be used in mixed poisonings with an organophosphorus compound
and a carbamate or if the type of insecticide is unknown.

Senyawa organophospat adalah
senyawa kimia yang mengandung
ikatan carbon-phospat
Carbamates adalah senyawa kimia
organik yang tersusun atas asam
carbamic
Menghambat kolinesterase
Orghanophospat > phosphorylasi
Carbamates > carbamilasi
Orghanophospat menimbulkan aging (terjadi
ikatan ireversibel orghanophospat-kolinesterse)
Terjadi Kolinergik Exsess