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8/4/2019 Poisoned of Corrosive Agent
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Poisoned of Corrosive Agent
Corrosive agent is a substance that may
causing damage on body, which if body ishit by this agent, it will causingprotoplasm coagulation, protein
precipitation and decomposition and alsowater absorption.
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Classification
Acid 1. Mineral acid
HCl (hydrochloride acid)
H2SO4 (sulfate acid)
HNO3 (nitrate acid)2. Organic Acid
- Carbolic Acid
- Oxalate Acid
- Acetate Acid
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Alkali :
Ammonia
KOH NAOH
Na carbonate
Ka carbonate
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Poisoned of HCl(Hydrochloride Acid)
Symptoms : Hyper salivation; convulsion ; delirium, body
paralysis
Chronics coryza; conjunctivitis; pharingitis,bronchitis
Fatal dosage : 15 - 20 ml condensed HCl
Post mortem:
Skin feels hard & chapped Cavity mucosa is cloudy white, until black becauseof corrosive reaction
Lungs oedem & congested if HCl vapor is breathed
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Poisoned of Sulfate Acid(H2SO4)
Thick & colorless liquid, if added with water, it will produceheat, and if hit to the skin, it will be black & burnt.
Symptoms: H2SO4 has a high affinity into water tissue will dried like burnt Bloated tongue, white coated Blood vomiting Chalk color teeth, do not gleam Bloated & chapped lips, there are trace of black acid drops from
the corner of lips and chin Hyper salivation; blue urine
Fatal dosage 5 - 100 ml
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Post Mortem
Stricture oesophagus
Black cavity, partly red inflammation, sometimesperforation
Corrosive marks at small intestine
Fattening at liver + kidney chronic
Congealed blood at blood vessels
Case : suicide
murder revenge sprinkle face with H2SO4
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Poisoned of Nitrate Acid (HNO3)
Clear, colorless liquid
Symptoms: Lips, tongue, teeth become yellow because of body protein
changing into xanthoprotein
Skin, cloths become yellow brownish yellow vomit materials
Distended abdomen painful
Oliguri until anurie
Lockjaw
Fatal dosage : 10 ml
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Post mortem
Skin & G.I.tract mucosa become yellow
Corrosive marking at cavity & duodenum
Oedem + congested at respiratory tract if enters
by respiration
Incident accident/suicide
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Poisoned of Carbolic Acid
Colorless Chrystal, if reacted with oxygen,it become pink. Sweet & hot like burnt
Symptoms:
Local arise insensible Feels burnt at G.I. tract White & harder mucosa at G.I tract CNS headache; dizzy; constriction pupil
Oppress respiration, sometimes pneumoniaA little green at urine because of oxidation
materials from carbolic acid
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Fatal dosage : 60 ml
Post mortem:
Pale/yellow skins until white and peeled off White corrosive marking at G.I. tract mucosa,
sometimes submucosa bleeding; carbolic acid odorfrom mouth.
Then cavity mucosa + small intestine become harder,brown, folded coarse, sometimes there are bleedingspots
Bigger kidney, inflammation marks with bleeding spots
Congested + oedem at brain
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Alkali :
Chloride ammonium
KOH
NaOH Carbonate ammonium
Carbonate potassium
Na carbonate
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Symptoms:
Bitter taste like soap
Diarrhea
Mucosa G.I.tract become black & slippery because mixed
of blood & detached parts Fatal dosage: ammoniac 5-10 gram
Post mortem:
Mucosa at G.I. tract become corrosive and necrosis, mucosa isslippery like soap
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Caustic soda (NaOH, KOH, CaOH,NH4OH)
Fatal dosage: 5 gr
Post mortem:
G.I.tract have inflammation marks + necrosis
Mucosa at G.I.tract slippery like soap, sometimesbleeding, black and brown
oedem + congested respiratory tract
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Death Cause of Corrosive Agent
Immediately : Neurogenic shock
respiration failure becauseof spasm & oedem glottis
Cavity perforation
peritonitis
Slow : Sepsis because of poison
absorption
Sticture oesophagus malnutrition
Chronic dyspepsia
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Irritant Agent
Poison that cause inflammation at digestiontracts
Classifications:
1. Inorganic: Non metal : Phosphor, organo-phosphor mixed, Chlorine,bromine, Iodine
Metal : Arsenic, Antimony, mercury, copper, tin, zinc,Bismuth
2. Organic: Poison from plants Poison from animals
3. Mechanical poison: glass powder
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Poisoned of Phosphor
2 kinds of phosphor: white & red phosphor.
White phosphor become yellow if it is hit by light,if reacted with oxygen, it will oxidized, produce
white smokes in the form of phosphor trioxides. Itis poisonous, usually used on chemical &fertilizer industry.
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Red phosphor doesnt poisonous, usually
used on matches industry.
How it works:
As a protoplasm poison & inhibit cellularoxidation.
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Acute Poisoned of Phosphor
Symptoms Stage 1 : few minutes few hours : painful, burnt from
throat until stomach, nauseous, vomit, greatly thirsty,diarrhea.
Stage 2 : during 2-3 days, usually asymptomatic.
Stage 3 : reappear symptoms, nauseous, vomit,diarrhea, yellow skins, bleeding at skin & mucousmembrane, ex: epistaksis, melena, hematuri, delirium,coma, and then circulation failure. Very few urine,contains blood, albumin, cylinder, which shows kidney
damage
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Fatal dosage : 50-120 gr
post mortem examination:
1. Yellow skin & bleeding spots
2. Cavity & small intestine mucosa are yellow, thick, erosion,
sometimes perforation. Cavity content smells garlic
3. Liver is yellow, brittle, bleeding and fat degeneration
4. Heart is pale, soft, and fattening
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Chronically Poisoned ofPhosphor
Usually because of breathing phosphor smoke onmatches industry.
Body parts : lower jaw which has caries. Lower jaw feelspain, then necrosis. This condition called phossy jaw. The
other bones also necrosis & usually spontaneous fracture. Death caused by lowering body endurance
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Arsenic Poisoned
Arsenic is poisonous when it is on salt forms:arsenic oxide (As2O3), arsenit, sulfide, organiccompounds.
Physically form : colorless, odorless, tasteless,like powder, doesnt dissolved on water, killing
affect on small amounts (30-300 gr).
Arsenic used on printing office, paint factory,insecticide, mouse killer, drugs.
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Type of Acute & ChronicallyPoisoned
Acute Poisoned:
Cellular metabolism is intruded because ofinhibition at sulfhidril enzyme system. Arsenic is
assumed as capillary poison & cause capillaryvenous dilatation.
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Symptoms
Burnt feels at larynx, pit of the stomach,
Greatly thirsty, nauseous, vomit, diarrhea,
Acute painful at abdomen,
Intestine spastic, black feces, because containblood & diarrhea like cholera
Few urine mixed with blood
Dilution & electrolyte balance trouble
Shock before death
Spasm, coma, dead.
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Death Cause
Shock because ofdehydration
Spasm because of
kidney failure Lungs oedem
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Post Mortem
Dehydration, concave eyes, uppermost bones,inflammation marks at G.I. tract, sometimesaccompanied with submucosa bleeding.
Cavity mucosa sometimes in form of thick mucus.
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Chronically Poisoned
Usually happened on industrial worker, paintfactory, insecticide using.
Symptoms : Stage 1 : body weight go down, digestion tract
trouble, nauseous, vomit Stage 2 : inflamed upper respiratory tract, husky &
coarse voice, brittle nail & pigmentation lines Stage 3 : sensory system start to be hit, dizzy,
hyperesthesia
Stage 4 : perifier neuritis & muscle atrophy. wristdrop or foot drop.
P i d f Pl b (ti h
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Poisoned of Plumbum(timah
hitam)o Resources :
Paint (wood, iron, or wall), battery, scarpiron.
o Work Mechanism: Intrude on hem synthesis, then delta-
aminolevulic acid, coproporphirin, &porphobilinogen at urine are increased.
o Autopsy results : GI tract mucosa are red and edema.
Hepar & Ren harder, tubulus degeneration.o Incident :
Accident, rarely murder/suicide.
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Poisoned of Mercury (Hg)Resources:
Thermo/Barometer industry, paint factory,lamp, explosive materials, medicine industry.
Work Mechanism:Inhibit sulfhidril enzyme works so intrude on
cells.Autopsy results:Acute : upper GI tract corrosion, soft mucosa
sp. Ulserasi. Congested, enlargement kidney,focal bleeding, Colon desac.sp.rectuminflamed.
Chronic : Fat degeneration at liver & heart,inflamed & bloated gums. There are bluebrown lines between teeth and gums.
Incident: Accident. Rarely murder/suicide.
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Poisoned of Cu(cuprum)
Resource:
On pharmacy as astringent, emeticum.
Autopsy results:
Acute :Yellow skin & conjunctiva, blue green mouth angle.
Ekskoriasi mouth. Blue cavity & intestine. Ulserasi colon.Perforation rectum. Congested, necrosis, and hemolyticorgans.
Chronic : like acute, along with liver necrosis & sirosis. cellsdegeneration along with enlargement kidney.
Incident:
Accident on industry, suicide ever known, rarely murder.
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Poisoned of Strychnine
Resources: Plant seeds and medicine.
Work mechanism: Inhibit cornu anterior medulla spinalis works.
Autopsy results: Stiff corps quickly arise.
Hyperemic until hemorrhages on cavity.
congested organs, medulla spinalis.
Incident: Accident, murder, rarely suicide.