Poisoned of Corrosive Agent

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.

Poisoned of Corrosive Agent

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