Toxicology

Dr. Harun Hudari, SpPD

DIVISION OF TROPICAL INFECTIOUS DISEASES
DEPARTMENT OF INTERNAL MEDICINE
SCHOOL OF MEDICINE, SRIWIJAYA UNIVERSITY
MOH. HOESIN HOSPITAL
PALEMBANG

Definition of Toxicology
- the basic science of poisons (old)
- the study of the adverse effects of
chemical agents on biological systems
(new)

The study of the adverse effects of a toxicant on

living organisms

Adverse effects
any change from an organisms normal state
dependent upon the concentration of active compound a
the target site for a sufficient time.
Toxicant (Poison)
any agent capable of producing a deleterious response i
a biological system
Living organism
a sac of water with target sites, storage depots and
enzymes

What is a Poison?
All substances are poisons;
there is none that is not a poison.
The right dose
differentiates a poison and a remedy.
Paracelsus (1493-1541)

WHAT TOXICOLOGISTS DO
-involved in the recognition, identification,
and quantitation of hazard
-develops standards and regulations to
protect health and the environment
- involved in safety assessment and use of
data as basis for regulatory control of hazards
- determines risk associated with use of chemicals

RISK ASSESSMENT
Hazard identification
Dose Response Assessment
Exposure Assessment
Risk Characterization

INTERRELATED COMPONENTS OF
THE RISK ASSESSMENT
chemical or physical agent
biological system
effect or response
exposure situation

AREAS OF TOXICOLOGY
(FIELDS OFSPECIALTY)

-descriptive
-mechanistic
-regulatory
-forensic
-clinical
-environmental

MAJOR FACTORS THAT INFLUENCE

TOXICITY
-route of administration
-duration and frequency of exposure
-dose or concentration

SPECTRUM OF UNDESIRED EFFECTS

-allergic reactions
-chemical allergies
-idiosyncratic reactions
-immediate vs. delayed toxicity
-reversible vs. irreversible toxicity
-local vs. systemic toxicity

INTERACTION OF CHEMICALS
Additive
Synergistic
Potentiation
Antagonism ( functional, chemical,
dispositional, receptor)

Dose
The amount of chemical entering the body
This is usually given as
mg of chemical/kg of body weight = mg/kg
The dose is dependent upon
* The environmental concentration
* The properties of the toxicant
* The frequency of exposure
* The length of exposure
* The exposure pathway

What is a Response?
The degree and spectra of responses depend upon the dose and
the organism--describe exposure conditions with description of
dose

Change from normal state

could be on the molecular, cellular, organ, or organism
level--the symptoms
Local vs. Systemic
Reversible vs. Irreversible
Immediate vs. Delayed
Graded vs. Quantal
degrees of the same damage vs. all or none

DOSE RESPONSE
-ASSUMPTIONS
-response is due to chemical administered
-the response is related to the dose
-there is a receptor site with which the
chemical interacts

DOSE RESPONSE
-ASSUMPTIONS (contd)
-the degree of response is related to
the concentration at the site
-the concentration at the site is related
to the dose administered
-has a quantifiable method of measuring and a
precise means of expressing the toxicity

Dose-Response Relationship:
As the dose of a toxicant increases,so does the
4
response.
RESPONSE
0-1 NOAEL
2-3 Linear Range
4 Maximum Response

DOSE

DOSE DETERMINES THE BIOLOGICAL RESPONSE

LD50

Quantal responses can be treated as gradient when data

from a population is used.
The cumulative proportion of the population responding
to a certain dose is plotted per dose--10-30 fold variation
w/in a population
If Mortality is the response, the dose that is lethal to 50%
of the population LD50 can be generated from the curve
Different toxicants can be compared--lowest dose is mos
potent

Individual Susceptibility
--there can be 10-30 fold difference in response
to a toxicant in a population
Genetics-species, strain variation, interindividual
variations (yet still can extrapolate between mammals-similar biological mechanisms)
Gender (gasoline nephrotox in male mice only)
Age--young (old too)
underdeveloped excretory mechanisms
underdeveloped biotransformation enzymes
underdeveloped blood-brain barrier

Individual Susceptibility
Age--old
changes in excretion and metabolism rates,
body fat
Nutritional status
Health conditions
Previous or Concurrent Exposures
additive
--antagonistic
synergistic

TOLERANCE
- state of decreased responsiveness to a toxic
effect of a chemical, resulting from previous
exposure
-dispositional tolerance; a decreased amount
of drug reaching the site
-cellular; reduced responsiveness of a tissue

Exposure: Pathways
Routes and Sites of Exposure
Ingestion (Gastrointestinal Tract)
Inhalation (Lungs)
Dermal/Topical (Skin)
Injection
intravenous, intramuscular, intraperitoneal
Typical Effectiveness of Route of Exposure
iv > inhale > ip > im > ingest > topical

RAPIDITY OF RESPONSE WITH

RESPECT TO ROUTE OF EXPOSURE

-intravenous
-inhalation
-intraperitoneally
-intramuscular
-intradermal
-subcutaneous
-topical

Exposure: Duration
Acute
< 24hr
Subacute 1 month
Subchronic 1-3mo
Chronic
> 3mo

usually 1 exposure
repeated doses
repeated doses
repeated doses

Over time, the amount of chemical in the body can build up

it can redistribute, or it can overwhelm repair and removal
mechanisms

ADME:
Absorption, Distribution,
Metabolism, and Excretion
Once a living organism has been exposed to a toxicant, the
compound must get into the body and to its target site in an
active form in order to cause an adverse effect.
The body has defenses:
Membrane barriers
passive and facilitated diffusion, active transport
Biotransformation enzymes, antioxidants
Elimination mechanisms

Absorption:
ability of a chemical to enter the blood
(blood is in equilibrium with tissues)

Inhalation--readily absorb gases into the blood stream via

the alveoli. (Large alveolar surface, high blood flow, and
proximity of blood to alveolar air)
Ingestion--absorption through GI tract stomach (acids),
small intestine (long contact time, large surface area--villi;
bases and transporters for others)
1st Pass Effect (liver can modify)
Dermal--absorption through epidermis (stratum corneum),
then dermis; site and condition of skin

Distribution:
the process in which a chemical agent
translocates throughout the body
Blood carries the agent to and from its site of action,
storage depots, organs of transformation, and organs of
elimination
Rate of distribution (rapid) dependent upon
blood flow
characteristics of toxicant (affinity for the tissue, and
the partition coefficient)
Distribution may change over time

Distribution:
Storage and Binding
Storage in Adipose tissue--Very lipophylic compounds
(DDT) will store in fat. Rapid mobilization of the fat
(starvation) can rapidly increase blood concentration
Storage in Bone--Chemicals analogous to Calcium-Fluoride, Lead, Strontium
Binding to Plasma proteins--can displace endogenous
compounds. Only free is available for adverse effects or
excretion

Target Organs:

adverse effect is dependent

upon the concentration of active compound at the
target site for enough time
Not all organs are affected equally
greater susceptibility of the target organ
higher concentration of active compound
Liver--high blood flow, oxidative reactions
Kidney--high blood flow, concentrates chemicals
Lung--high blood flow, site of exposure
Neurons--oxygen dependent, irreversible damage
Myocardium--oxygen dependent
Bone marrow, intestinal mucosa--rapid divide

Target Sites:
Mechanisms of Action
Adverse effects can occur at the level of the molecule, cell,
organ, or organism
Molecularly, chemical can interact with
Proteins Lipids DNA
Cellularly, chemical can
interfere with receptor-ligand binding
interfere with membrane function
interfere with cellular energy production
bind to biomolecules
perturb homeostasis (Ca)

Metabolism:
adverse effect depends on the concentration of active
compound at the target site over time

The process by which the administered chemical (parent

compounds) are modified by the organism by enzymatic
reactions.
1o objective--make chemical agents more water soluble
and easier to excrete
decrease lipid solubility --> decrease amount at
target
increase ionization --> increase excretion rate -->
decrease toxicity
Bioactivation--Biotransformation can result in the
formation of reactive metabolites

Biotransformation

Key organs in biotransformation

LIVER (high)
Lung, Kidney, Intestine (medium)
Others (low)
Biotransformation Pathways
* Phase I--make the toxicant more water soluble
* Phase II--Links with a soluble endogenous
agent (conjugation)

Excretion:
Toxicants are eliminated from the body by several
routes

Urinary excretion
water soluble products are filtered out of the blood by th
kidney and excreted into the urine
Exhalation
Volatile compounds are exhaled by breathing
Biliary Excretion via Fecal Excretion
Compounds can be extracted by the liver and excreted
into the bile. The bile drains into the small intestine and
is eliminated in the feces.
Milk, Sweat, Saliva

Management of Toxicology

Objectives
General approach to the poisoned
patient
Toxidromes
Specific antidotes
Decontamination and enhanced
elimination

General Approach

ABCs
History
Physical examination
Labs, imaging
Diagnosis, antidotes
Disposition

Airway

Airway obstruction can cause death after poisoning

Flaccid tongue
Aspiration
Respiratory arrest

Evaluate mental status and gag/cough reflex

Airway interventions

Sniffing position
Jaw thrust
Head-down, left-sided position
Examine the oropharynx
Clear secretions
Airway devices: nasal trumpet, oral airway

Intubation?
Consider naloxone first

Breathing

Determine if respirations are adequate

Give supplemental oxygen
Assist with bag-valve-mask
Check oxygen saturation, ABG
Auscultate lung fields
Bronchospasm: Albuterol nebulizer
Bronchorrhea/rales: Atropine
Stridor: Determine need for immediate intubation

Circulation

IV access
Obtain blood work
Measure blood pressure, pulse
Hypotension treatment:
Normal saline fluid challenge, 20 mL/kg
Vasopressors if still hypotensive
PRBCs if bleeding or anemic

Hypertension treatment:
Nitroprusside, beta blocker, or nitroglycerin

Continuous ECG monitoring

Assess for arrhythmias, treat accordingly

Supportive Care

Foley catheter
Rectal temperature
Accucheck, treat hypoglyemia
Coma cocktail
Thiamine: 100 mg IV, before dextrose
Dextrose: 50 grams IV push
Naloxone: 0.01 mg/kg IV

Supportive Care
Treat Seizures
Lorazepam 2 mg IV, may repeat as needed
Dilantin 10 mg/kg IV

Control agitation
Haldol 5-10 mg IM
Ativan 2-4 mg IM or IV
Geodon 20 mg IM

Think about trauma

REASSESS
. . . frequently

History/Anamneses

What, when, how much, why?

Rx, OTC, herbals, supplements, vitamins
Talk to family, friends, EMS
Pill bottles, needles, beer cans, suicide not
Call pharmacy
Allergies, medical problems

Physical examination

Vital signs: BP, HR, RR, T, O2 sat

Mouth: odors, mucous membranes
Pupils
Breath sounds
Bowel sounds
Skin
Urination/defecation
Neurologic exam

Essential Laboratory Tests

Electrolytes
Glucose
BUN and creatinine
LFTs, CK
Urinalysis, urine drug screen
Etoh, alcohol screen
Serum osmolality
Acetaminophen, salicylates
Specific drug levels
Pregnancy test

Anion Gap
Na (HCO3 + Cl)
Normal: 8-12 mEq/L
Causes:

Methanol
Uremia
DKA
Paraldehyde, phenformin
Iron, isoniazid, ibuprofen
Lithium, lactic acidosis
Ethylene glycol
Strychnine, starvation, salicylates

Osmolar Gap

Calculated osmolality measured osmolality

2(Na) + glucose/18 + BUN/2.8
Normal = 285-290 mOsm/L
Gap > 10 mOsm/L suggests the presence of extra
solutes:
Ethanol, methanol
Ethylene glycol, isopropyl alcohol
Mannitol, glycerol

Clinical Pearl: Anion gap acidosis with an osmolar

gap should suggest methanol or ethylene glycol
poisoning

Electrocardiogram

Prolonged QRS

Sinus bradycardia/AV block

TCAs
Phenothiazines
Calcium channel blockers
Beta-blockers, calcium channel
blockers
TCAs
Digoxin
organophosphates

Ventricular tachycardia

Cocaine, amphetamines
Chloral hydrate
Theophylline
Digoxin
TCAs

Diagnosis
May not identify ingested substance(s)
Provide ABCs and supportive care
Give antidote when appropriate

Disposition

Case-based
ICU admission
Period of observation
Psychiatric evaluation

Toxidromes

Opioids
Respiratory depression
Miosis
Hypoactive bowel sounds

Sympathomimetics

Hypertension
Tachycardia
Hyperpyrexia
Mydriasis
Anxiety, delirium

Clinical Pearl: Sweating differentiates sympathomimetic

and anticholinergic toxidromes

Cholinergics
Organophosphates
Irreversibly bind cholinesterases

Carbamate
Reversibly bind cholinesterases, poor CNS penetration

Muscarinic and nicotinic effects

Pesticides, nerve agents

Military personnel
Field workers, crop dusters
Truckers
Pest control, custodial workers

Antidote
Atropine for muscarinic effects
Pralidoxime reverses phosphorylation of cholinesterase

Cholinergic Toxidrome
Diarrhea
Salivation
Urination Lacrimation
Miosis
Urination
Bradycardia
Defecation
Bronchospasm GI upset
Emesis
Emesis
Lacrimation
Limp
Salivation, sweating

Anticholinergics

Atropine
Scopolamine
Glycopyrrolate
Benztropine
Antispasmotics

Dicyclomine
Hyoscyamine
Oxybutynin
clidinium

TCAs
Mydriatics

Antihistamines

Chlorpheniramine
Cyproheptadine
Hydroxyzine
Diphenhydramine
Meclizine
promethazine

Antipsychotics
Clozapine
Olanzapine
Thioridazine

Anticholinergic Toxidrome

Dry mucus membranes (Dry as a bone)

Mental status changes (Mad as a hatter)
Flushed skin (Red as a beet)
Mydriasis (Blind as a bat)
Fever (Hot as a hare)
Tachycardia
Hypertension
Decreased bowel sounds
Urinary retention
Seizures
Ataxia

Antidotes

Acetaminophen
N-acetylcysteine
Organophosphates
Atropine, pralidoxime
Anticholinergic
physostigmine
Arsenic, mercury, gold
dimercaprol
Benzodiazepines flumazenil
Beta blockers
glucagon
Calcium channel block
calcium
Carboxyhemoglobin
100% O2
Cyanide
nitrite, Na thiosulfate
Digoxin
digoxin antibodies

Antidotes

Ethylene glycol
fomepizole, HD
Heparin
protamine
Iron deferoxamine
Isoniazid pyridoxime
Methanol
fomepizole, HD
Methemoglobin methylene blue
Opioids
naloxone
Salicylate alkalinization, HD
TCAs
sodium bicarbonate
Warfarin FFP, vitamin K

Decontamination

Principles of Decontamination
External
Protect yourself and others
Remove exposure
Irrigate copiously with water or normal
saline
Dont forget your ABCs

Internal
Patient must be fully awake or
intubated
Most common complication is
aspiration
Very little evidence for their use

Decontamination
Skin
Protect yourself and other HC
workers
Remove clothing
Flush with water or normal saline
Use soap and water if oily
substance
Chemical neutralization can
potentiate injury
Corrosive agents injure skin and
can have systemic effects

Decontamination
Eyes

remove contact lens

Flush copiously with water or normal saline
Use local anesthetic drops
Continue irrigation until pH is normal
Slit lamp and fluorescein exam

Decontamination
Inhalation
Give supplemental humidified oxygen
Observe for airway obstruction
Intubate as necessary

GI Decontamination

Syrup of ipecac
Within minutes of ingestion
Aspiration, gastritis, Mallory-Weiss tear, drowsiness
Rarely, if ever, given in ED

Gastric lavage

Does not reliably remove pills and pill fragments

Used 30-60 minutes after ingestion
Useful after caustic liquid ingestion prior to endoscopy
Not used for sustained release/enteric coated ingestions
Perforation, nosebleed, vomiting, aspiration

Recent studies suggest that activated charcoal alone is just as

effective as gut emptying followed by charcoal.

GI Decontamination
Activated charcoal
Limits drug absorption in the GI tract
Within 60 minutes of ingestion
Patient must be awake or intubated
Vomiting, aspiration, bezoar formation
Contraindication: bowel obstruction or ileus
with distention
1 gram/kg PO or GT

Activated Charcoal
Not good for:

Lithium
Iron
Alcohols
Lead
Hydrocarbons
Caustics

GI Decontamination
Cathartics

Hasten passage of ingestions or AC

Contraindications: obstruction or ileus
Severe fluid loss, hypernatremia, hyperosmolarity
10% magnesium citrate 3ml/kg or 70% sorbitol 1-2
./kg

Whole bowel irrigation

Large ingestions, SR or EC tablets, packers (ex.
cocaine)
Contraindications: obstruction or ileus
Aspiration, nausea, may decrease effectiveness of
charcoal

Intoksikasi Insektisisda Fosfat Organik

o Nama lain (IFO):
-Insektisida organo fosfat atau
-Insektisida cholinesterase inhibitor.

IFO merupakan insektisida poten yang paling banyak digunakan

dalam pertanian dengan toksisitas tinggi

Etiologi
IFO dibagi dua macam: IFO murni & gol. Carbamate.
Beberapa contoh IFO: Malathion, Diazinon, Basudin, Paraoxon,
Phosdrin, Raid, Systox, dll.
Salah satu contoh gol.carbamate: Baygon

Gambaran Klinik
Yang paling menonjol adalah kelainan visus,
hiperaktivitas kelenjar ludah /keringat, saluran makan dan
kesukaran bernafas.
Ringan: anoreksi, nyeri kepala, lemah, rasa takut, tremor
lidah & kelopak mata, miosis pupil
Sedang: nausea, muntah, kejang/kram perut,
hipersalivasi, hiperhidrosis, fasikulasi otot, bradikardi.
Berat: diare, pupil pin-point, reaksi cahaya (-), sesak,
sianosis, edema paru, inkontinensia urin & alvi, konvulsi,
koma, blok jantung, akhirnya meninggal.

Diagnosis
Ditegakkan atas dasar gambaran klinis yang khas.
Laboratorium rutin tidak banyak menolong.
Pengukuran sel darah merah dan plasma, penting untuk
memastikan diagnosis keracunan IFO akut maupun
kronis.

Pengobatan:
a. Resusitasi
b. Eliminasi/Bilas lambung melalui NGT
c. Antidotum:
- Atrofin Sulfat (SA), menghambat efek
akumulasi AKh pada tempat penumpukan.
- Dosis; mula-mula bolus iv 1-2,5 mg,
dilanjutkan 0,5-1 mg setiap 5-10-15 menit,
sampai timbul gejala atropinisasi. Kemudian
interval diperpanjang setiap 15-30-60 menit,
selanjutnya setiap 2- 4-6 dan 12 jam.

- SA dihentikan minimal setelah 2 x 24 jam

- reaktivator KhE-bekerja memotong ikatan
IFO-KhE, hingga timbul reaksi enzim KhE.
Hanya bermanfaat pada keracunan IFO.
Dosis; 1 gram iv pelan (10-20 menit dalam
infus), dapat diulang setelah 30 mnt
sebanyak 2 x 24 jam.

INTOKSIKASI AMFETAMIN
Sering terjadi pada usia muda, di akhir pekan, berdansa,
tripping, menggerakan kepala terus.
Bersifat patologik, paling sedikit 1 bulan
Ectasy (XTC)
Pertama kali di Jerman (1914)
Tergolong amfetamin
Kelompok halusinogenik : mampu membuat ilusi visual,
distorsi sensori, synesthesia (mampu melihat suara dan
membau warna) despersonalisasi dan derealisasi
Nama kimia MDMA
(methylene dioxy methamphetamine)

Efek farmakologik
Bentuk : tablet, bubuk, injeksi
System dopaminergik berakibat aktif dan penuh energi. Efek
serotonergik menimbulkan disorientasi, distorsi persepsi dan
halusinogenik
Efek timbul 20-30 menit, berakhir setelah 4-48 jam
Dosis letal beberapa kali dosis halusinogenik
Sering didapat dalam kombinasi dengan narkotik, kafein,
lidokain, aspirin dll.

Diagnosis
Anamnesis :
Ada riwayat konsumsi obat halusinogenik
Gejala : (ringan-berat)
Nyeri kepala, palpitasi, sesak, nyeri dada
Parestesi, banyak omong, euphoria, empati
Terlalu percaya diri, insomnia
Kadang perubahan persepsi visual ringan
Keracunan Ringan :
Mudah tersinggung, mulut kering, palpitasi
Hipertensi ringan, gelisah, susah beristirahat
Tremor, midriasis dan flushing

Keracunan sedang :
Rasa takut, agitasi, mual, muntah, nyeri perut
Kejang otot, hiperrefleksi, diaforesis, takikardi
Hipertensi, hipertermi, panik dan halusinasi
Keracunan berat :
Delirium, kejang-kejang, gejala fokal SSP (perdarahan
intrakranial), koma, aritmia
Otot kaku, hipertensi, gangguan hemostasis, gagal nafas,
gagal ginjal akut, meninggal

Gejala penghentian obat tiba-tiba

Kelelahan otot menyeluruh, hipertermia, mimpi buruk, depresi
agitatif dan usaha bunuh diri
Flash back, Insomnia, hipersomnia
Perasaan dingin seluruh tubuh
Perasaan takut yang berlebihan > 2 minggu
Analisis laboratorium
Bahan: darah, urine, cairan lambung
Amfetamin dalam urin bertahan 2 hari
Kasus keracunan berat: periksa fungsi ginjal, gas darah, elektrolit,
sakar darah, urinalisis, EKG

Prinsip pengobatan menghindari kontak/eliminasi obat

dengan cara :
Mencegah konsumsi obat tersebut
Beri norit / obat katarsis
Rangsang muntah bila kesadaran baik
Bilas lambung
Diuresis paksa (karena obat ini di ekskresikan ke ginjal)

Pengobatan simptomatis
Ansietas : diazepam 0,05-0,1 mg/kgBB IV atau oral. Dapat
diulang 5-10 menit
Agitasi/psikosis : haldol 5-19 mg iv. Dapat diulang 10-60 menit
Hipertensi berat : beta blocker/vasodilator
Takikardi supraventrikular dengan iskemia jantung : beta blocker
Iskemia miokard : morfin, nitrat
Hipertermia : ruangan dingin
Koagulopati : heparin
Perawatan intensif :
Kasus berat dan kesadaran turun

INTOKSIKASI OPIAT
Umum digunakan untuk mengatasi nyeri melalui efek
depresi pada otak
Golongan opiat : morfin, petidin, heroin, kodein
termasuk narkotika, barbiturat, meprebamat,
benzodiazepin, etanol dan putau
Penyalahgunaan obat :
New York (1970) : 1200 meninggal karena
overdosis
USA: 10.000 meninggal karena overdosis

Farmakologi Opiat
Setelah pemberian dosis tunggal tunggal heroin (putaw),
dalam 6-10 menit akan dihidrolisis oleh hati menjadi 6monosetil morfin setelah itu diubah menjadi morfin
Selanjutnya diubah menjadi Mo-3-monoglukoronid dan Mo6 monoglukoronid yang larut dalam air (dapat dires dalam
urine)
Karena heroin larut dalam lemak : dapat melalui sawar otak
dalam waktu yang cepat

Diagnosis
Gejala klinis khas (pin point, depresi nafas, membaik
setelah pemberian nalokson)
Kadang ditemukan bekas suntikan (needle track sign)
Laboratorium : tidak selalu seiring dengan gejala klinis
Pemeriksaan kualitatif urine : cukup efektif untuk
memastikan diagnosis

Gambaran Klinis
Umumnya cenderung terjadi penurunan kesadaran (sampai
koma)
Dosis toksik :
Selalu menyebabkan penurunan kesadaran mengantuk sampai
koma, bicara cadel
Pin poin pupil, dilatasi pupil terjadi pada anoksia yang berat
Pernafasan pelan (depresi pernafasan), sianosis, nadi lemah,
hipotensi, spasme saluran cerna dan bilier. Edema paru dan kejang

Keadaan putus opiat

A. Salah satu keadaan berikut :

Penghentian atau penurunan dosis opiat

Pemberian antagonis opiat

B. Tiga (atau lebih) berikut ini yg berkembang beberapa hari

setelah A.
1). Mood disforik, 2). Mual muntah, 3)nyeri otot
4)lakrimasi/rinorea, 5)dilatasi pupil, piloereksi,
keringat, 6)diare, 7)menguap, 8)demam,9)insomnia

C. Gejala B menyebabkan gangguan fungsi sosial, pekerjaan

atau fungsi lain

Kematian
2-4 jam setelah pemakaian oral/subkutan
IV gejala lebih berat :
Hipertemia, aritmia jantung, hipertensi, bronkospasme
Akut Tubular Nekrosis (ATN) karena rabdomiolisis dan
mioglobulinuria dan gagal ginjal
Kulit warna kemerahan
Lekositosis dan hipoglikemia

Prinsip Penatalaksanaan

Penatalaksanaan kegawatan

Penilaian klinis

Dekontaminasi racun

Pemberian antidotum

Terapi suportif

Observasi dan konsultasi

Rehabilitasi

Penatalaksanaan kegawatan :
Nilai tanda vital seperti jalan nafas, sirkulasi,
kesadaran
Tindakan resusitasi yang umum seperti: airways
(A), Breathing (B), Circulation (C)

Penilaian klinis :
Perhatikan adanya koma, kejang, henti jantung,
henti nafas dan syok
Anamnesis :

 Pemeriksaan fisis :
Cari tanda atau kelainan fungsi otonom seperti
tekanan darah, nadi, pupil, keringat, air liur dan
peristaltic usus
Misal pada gejala simpatis (simpatomimetik):
ditemukan delirium, paranoid, takikardi, hipertensi,
hiperpireksia, diaforesis, midriasis, aritmia dan
kejang

Pengobatan
Nalokson 0,4-2,0 mg. Dosis dapat diulang pada keracunan
yang berat dengan panduan klinis. Efek sekitar 2-3 jam. Bila
respon tidak ada setelah dosis total 10 mg maka diagnosis
intoksikasi opiat dikaji ulang
Edema paru : nalokalion
Hipotensi : dopamine 2-5 ug/kgBB/menit
Jangan dimuntahkan bila intoksikasi oral
Kumbah lambung: segera setelah intoksikasi oral, awasi jalan
nafas
Kejang : diazepam iv 5-10 mg. Diulang bila perlu

Lama Waktu Deteksi Urine Beberapa Jenis

Opiat
Jenis obat
Amfetamin

Waktu deteksi
2 hari

Barbiturat

1 hari (Short acting)

3 mgg (long acting)

Benzodiazepin
Kokain

3 hari
2-4 hari

Kodein
Heroin

2 hari
1-2 hari

Methadone
Morfin

3 hari
2-5 hari