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Manajemen Intoksikasi Dan Keracunan Gas

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Management of Intoxication and

Gas Poisoning

Mohamad Arif
Internal Medicine Departement
Faculty of Medicine UNISSULA Semarang
2019
Definition

• poison :any substance that causes a harmful


effect when administered, either by accident or
by design, to a living organism.
• toxic properties of the chemical
• the dose administered but also on
• individual and interspecific variation
Air pollutan
• Gaseous Pollutants These substances are gases at
normal temperature and pressure as well as vapors
evaporated from substances that are liquid or solid.
Example:
carbon monoxide (CO) and carbon dioxide
hydrocarbons
hydrogen sulfide (H2S)
nitrogen oxides (NxOy)
ozone (O 3 )
and other oxidants, sulfur oxides (SxOy).
Particulate Pollutants :
Fine solids or liquid droplets can be suspended
in air.
1. Dust. Relatively large particles about 100 μm that come
directly from substances being used (e.g., coal dust, ash,
sawdust, cement dust, grain dust).
2. Fumes. Suspended solids less than 1 μm in diameter usually
released from metallurgical or chemical processes (e.g., zinc
and lead oxides).
3. Mist. Liquid droplets suspended in air with a diameter less
than 2.0 μ m (e.g., sulfuric acid mist).
4. Smoke. Solid particles (0.05 – 1.0 μ m) resulting from
incomplete combustion of fossil fuels.
5. Aerosol. Liquid or solid particles ( < 1.0 μ m) suspended in
air or in another gas.
Acute vs chronic toxicity

• acute toxicity can be defined as toxicity elicited


immediately following short - term exposure to a
chemical
• High - level, short - term exposure pollutant
• In contrast to acute toxicity, chronic toxicity is
characterized by prolonged exposure and sub-lethal
effects elicited through mechanisms that are
distinct from those that cause acute toxicity.
factors affecting inhalation
toxicity:
• Agent:
 concentration of inhaled toxin,
 duration of exposure, enclosed space,
 particle size and water solubility
• Host :
 elderly or younger patients
 allergic or nonallergic bronchospastic response,
 exertional state or metabolic rate of the victim,
 history of smoking
 underlying lung debilitating illness, particularly underlying
reactive airway
Pathogenesis inhalation toxicity

• may directly injure the pulmonary epithelium at


various levels of the respiratory tract
• wide range of disorders from tracheitis and
bronchiolitis to pulmonary edema.
• They may also resulting in systemic toxicity.
• Thus, determining the mechanism of respiratory
insufficiency, whether it is a result of direct injury
of respiratory tract or systemic toxicity, is difficult.
Inhalasi bahan toksik
Akut : ALI /ARDS
Efek lokal
Aldehid Kronik :
Nitrogen dioksida Fibrosis
Asma
Bronkiektasis,
PPOK

Efek sistemik : Karbon monoksida, Klorin


Inhalasi agen toksik

Kronik Akut

Penyakit paru obstruksif Iritasi mukosa


Asma/Rhinitis Erosi mukosa
Bronkiektasis Keruskan mukosa
Fibrosis Pneumonitis

ALI/ARDS
 Acute Respiratory Distress Syndrome
(ARDS)

Adalah suatu sindroma gagal nafas


akut akibat kerusakan sawar membran
kapiler alveoli , sehingga menyebabkan
edema paru akibat peningkatan
permeabilitas.
Bentuk ARDS yang lebih ringan adalah
ALI (acute lung injury).
Inhalasi bahan toksisk
Analisa gas darah
12-24 jam Hipoksemia menetap
PO2 < 60 mmhg
PO2/FiO2 < 200
AADO2 > 300
Distres pernafasan
Perburukan sesak nafas
Takipneu X R Thorak
Infiltrat difus bilateral

ARDS
Tekanan baji kapiler paru/PCWP < 18
mmhg
ALI jika PO2/FIO2 200-300 mmhg
Gejala klinis

• Takipneu
• Retraksi intercostal
• Ronki baasah kasar
• Hipotensi
• Febris
• Gagal multi organ
Traum Kerusakan alveolar/endotel vaskuler
a
Aktivasi kaskade inflamasi

Inisiasi : pelepasan mediator inflamasi ke paru


dan sistemik
Amplifikasi: Netrofil teraktivasi tertarik ke
dan tertahan di paru
Injuri: Netrofil melepaskan mediator inflamasi
merusak paru dan merangsang inflamasi

Kerusakan membran alveolar-kapiler


Kerusakan membran alveolar-kapiler

Peningkatan permeabilitas
membran
Aliran cairan ke alveoli

Kerusakan surfaktan dan alveoli lanjut:


1. Fase eksudatif
2. Fase proliferatif
3. Fase fibrosis
Eksudatif :
 Edema interstisial dan alveolar
 Nekrosis sel pneumosit
 Terlepasnya membran hialin
 Pembengkakan sel endotel
 Pembentukan membran hialin
 Hipertensi pulmoner

Proliferatif: proliferasi sel epitel pneumosit

Fibrosis : peningkatan kolagen terbentuknya


fibrosis
Kriteria Diagnosis ARDS:

1.Riwayat pencetus.
2.Hipoksemia refrakter dengan terapi oksigen
PaO2/FiO2 <200 .
3.X Foto thorak : infiltrat bilateral difus.
4.Tidak ada gejala edema paru kardiogenik
dan tekanan baji ≤ 18 mmHg.
Penatalaksanaan ARDS
1. Terapi oksigen
2. Intubasi dan ventilasi mekanis
3. Terapi untuk memperbaiki oksigenasi
- Vasodilator a. pulmoner ( nitrit okside, prostasiklin )
4. Terapi pengganti surfactan
5. Terapi anti inflamasi : Glukokortikoid
6. Tatalaksana umum :
- Optimalisasi hemodinamik : terapi cairan, koreksi
anemia
- Nutrisi : enteral feeding
7. Terapi penyakit dasar
Keracunan karbonmonoksida (CO)

• Gas yang tidak berwarna, tidak berasa, tidak


berbau,tidak mengiritasi
• Pembakaran di ruangan tertutup atau dari asap knalpot
mobil/motor
• Batas paparan yang diperbolehkan 35 ppm 8 jam/ hari
kerja
• Paparan 1000ppm dalam beberapa menit dapat
menyebabkan pembentukan COHb 50%
CO

Berikatan dengan Hemoglobin 250x lebih kuat dari


O2

O2 terlepas dari Hemoglobin COHB

Pasokan O2 turun Interaksi protein heme

Kurva penguraian HbO2 bergeser


kekiri
Pengurangan pelepasan O2 dari
Hipoksia darah kejaringan
Keracunan karbonmonoksida (CO)

enzim sitokrom oksidase


CO

Oksidasi mitokondria ATP


Gejala klinis
Akut
1. Ringan ( COHb : 10-30 %): Sakit kepala daerah
temporal, sesak, pusing
2. Sedang ( COHb : 30-50 % ) :Nyeri kepala hebat,
kelelahan, pusing,mual, muntah, sinkop, takikardia,
takhipnea
3. Berat ( COHb : 50-80 % ) : Sinkop, kejang, koma,
gangguan kardiovaskuler, kematian

Kronik
Parestesi jari-jari, memori menurun, Romberg sign +,
perubahan mental

Pulse Oksimetri akan tampak normal karena COHb memiliki


spektrum serapan yang mirip dengan oksihaemoglobin.
Management CO toxicity

• avoid CO gas exposure


• CO is only removed from the body through
displacement by O2; therefore use high
concentrations of oxygen
• Raise the PaO2 as high as possible, intubate and
100% O2 if necessary

Oxford Handbook of Respiratory Medicine, 1st Edition


Terima kasih

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