The document discusses various agricultural poisons, primarily focusing on organophosphorus compounds and their effects on the human body, including the mechanism of action, absorption routes, symptoms of poisoning, treatment options, and postmortem appearances. It details the symptoms of acute and chronic poisoning, the importance of antidotes like atropine and oximes, and highlights the medico-legal implications of poisoning incidents. Additionally, it mentions other types of pesticides, such as carbamates, organochlorines, paraquat, and phosphides, outlining their toxicity, symptoms, and treatment modalities.

1. AGRICULTURAL
POISONS
Dr. SIDHARTH.S

2. ORGANOPHOSPHOROUS COMPONDS
• Consists of Central Phosphorus Molecule. With B & B’ Basic groups and another
bond of either Oxygen or Sulphur.
• The fourth bond is either Alkyl or Aryl Group.
• So they are either Alkyl or Aryl Phosphates.
• HETP (Hexa Ethyl Tetra Phosphate)
• TEPP ( Tetra Ethyl Pyrophosphate)
• OMPA (Octa Methyl Pyrophosparamide)
• Malathion etc.
• Parathion.
• Methyl Parathion.
• Paraoxon.
• Diazinon.

3. ABSORPTION OF OP Compounds:
• Absorbed through the intact skin and mucous membrane, gastro-intestinal tract and by inhalation.
• Mixing it with AROMAX gives it a characteristic kerosene like odour.
MECHANISM OF ACTION:
• Acetyl Choline, produced in the body, is hydrolysed by Acetyl Cholinesterase (AChE) to Acetic Acid
and Choline.
• The OP Compounds inactivate the AChE by PHOPHORYLATION, resulting in accumulation od Acetyl
Choline in the body.
• AChE has two sites:
ESTERIC SITE
ANIONIC SITE
Organophosphates act on this site.
True Cholinesterases
Red Cells, Neuro muscular Jn &
Brain
PseudoCholinesterases
Plasma

4. Initially, the binding of organo
phosphorous is due to hydroststic
attraction .
REVERSIBLE REACTION
Firm binding occurs when a H –ion
is transferred from the complex.
IRREVERSIBLE REACTION.
Treatment with antidote, if initiated, it has to be done before firm binding.
Within 24 hours of poisoning.

5. Signs & Symptoms:
• The clinical manifestations of Organophosphates are due to an overdose of Acetyl Choline in the body.
MUSACRINIC EFFECTS NICOTINIC EFFECTS CNS MANIFESTATIONS
Salivation.
Lacrimation.
Urination( Incontinence due to stimulation of bladder).
Defecation.
Gastro intestinal distress.
Emesis.
• Pupils constricted.
• In Eye, ciliary muscles are constricted & suspensory ligaments are relaxed; so lens bulges out into
anterior chamber- blurring of Vision.
• Severe Lacrimation in severe cases- Chromolachryorrhoea (due to inhibition of porphyrin metabolism
resulting in accumulation of porphyris in lacrimal glands).
• Respiratory system: Increased secretions, bronchoconstriction, dyspnoe, Pulmonary edema.
• CVS symptoms: Bradycardia, Hypotension.
• Acts on PreGanglionic
NMJ
• Muscle twitching,
cramps and muscle
fatigue.
• Fasiculations.
• Headache, Restlessness,
confusion, drowsiness, coma.
• Depression of Cardiac and
Respiratory centres.
• Death due to Respiratory Failure.

6. • Other Neurological Manifestations:
 Type 1 Paralysis:
• Acute paralysis within 24-48 Hours.
• Due to persistent depolarization at NMJ due to
blockade od AChE.
• Fasiculations, Cramps, Weakness, Paralysis of
Respiratory muscles.
• Respiratory failure.
• Rx: Atropine.
 Type 2 Paralysis:
• 2-4 days after resolution of acute cholinergic
symptoms.
• Manifests as Paralysis & Respiratory distress.
• Due to Neuromuscular transmission defect or
toxin induced muscle instability or inadequate
treatment.
• Weakness of Proximal Limb muscles, Neck
Flexor, Resp Muscles & Cranial nerve palsy.
• Delayed deaths +/-
• Do not respond to Atropine / Oximes.
 Type 3 Paralysis:
• 1-4 weeks after exposure to OP
Compounds.
• Paralysis of lower extremities, foot drop &
numbness.
• Gradually progress upwards.
• Parasthesia +/-.
• Sensory symptoms subside in 1-2 months,
but paralysis persists.
• Do not respond to Atropine / Oximes.

7. Other sequelae in survivors:
• Urinary incontinence, demyelination of optic nerve, visual defects, peripheral neuropathy, extra
pyramidal symptoms, loss of memory and lethargy.
• Chronic organophosphate induced neuropsychiatric disorder (COPIND)
Combination of psychiatric, neurological & extrapyramidal symptoms that occur late, but long lasting.
Fatal Dose varies according to the type of OP Compound ingested.
Fatal Period: death within 24 hours. (can occur as early as 30 mins after ingestion if dose is high).
Death in OP Poisoning:
1. Respiratory failure due to paralysis of respiratory centre.
2. Paralysis of respiratory muscles & bronchospasm due to direct action of ACh here).
3. A-V Blockade leading to Cardiac Arrest.

8. Symptoms
in
OPC
Poisoning:

9. Diagnosis:
Cholinesterase Activity
• Estimation of cholinesterase activity- both red cell and
plasma cholinesterases.
• Ch-E activity reduced to 22 – 88 %.
Type of Cholinesterase Normal Value
Red cell Cholinesterase 77-142
Plasma Cholinesterase 41-140
• Pseudo ChE levels are more sensitive and falls rapidly than Red
Cell ChE.
• True ChE activity is better and of more diagnostic value.
• Prognosis based on the level of ChE Activity.
Chemical Analysis
• Detected in Blood using Thin Layer
Chromatography or Liquid Gas
Chromatography.
• Estimation of para nitro phenol is
diagnostic for Parathion Poisoning.

10. Treatment:
• In GENERAL, clothes of the patient to be removed, body to be washed with soap & water to prevent
cutaneous absorption of OPC.
• Irrigation of eyes, if contaminated.
• Maintain patent airway.
• Oxygen therapy if cyanosis +.
• Stomach wash with 1:1000 KMnO4 Soln. if the poison was ingested; with or without activated
charcoal.
• Atropine Sulphate reverses effect of Ach. Acts as a physiological antidote
 Reverses the Muscarinic Effects of ACh at the Muscarinic receptors. So there is decreased
Parasympathetic activity.
 No effect on Nicotinic symptoms as it do not act on those receptors. So, no action a NMJ.
 DOSE: 2-4 mg every 10-15 mintues till signs of atropinization appears
 Dilatation of pupil and decrease of secretions.

11. • Treat with Oximes, as specific antidotes.
• React with phosphate moiety of OP-AChE complex and get phosphorylated.
• AChE is released from the complex and thus reactivated.
• Decreases the Muscarinic, nicotininc and CNS effects within 10-40 minutes.
• Oximes to be administered as early as possible, before the complex becomes irreversible.
• Not beneficial if given after 48 hours of poisoning. By this time, the complex will become irreversible.

12. • Postmortem Appearence:
Face: Congested
Conjunctivae: Congested
Froth in Mouth and nostrils.
Stomach contents smell of
kerosene, if the content
ingested contains Aromax.
Lungs: Congested & edematous.
Brain: Congested.
All Internal Organs are congested.
Heart: Petechial Hemorrhages
on Pericardial surface.

13. Chronic Poisoning is seen in persons spraying the compound in agricultural field, due to
inhalation.
• Manufacture and packing of OPC.
• Symptoms: Muscle weakness lethargy, anxiety, confusion, muscle cramps, parasthesias.
Circumstances of Poisoning:
Suicide
Most Common.
Accidental
In sprayers & children.
Homicide
Rare.
Can occur if mixed in
alcohol or other soft
drinks.

14. MEDICO LEGAL IMPORATNCE OF OPC Poisoning.
Suicide Alone or mixed with some other poison.
Homicide Rare- due to its strong smell and bad taste.
Accidental Quite common. Eg: Kerala Food Tragedy of 1958; Bihar mid-day meal tragedy of 2013.
Warfare Two main groups of OPCs used in Warfare are G & V series. (see War Gases).
• Organophosphate compounds resists PUTREFACTION.
Can be detected in Viscera for sometime even after death.
• OP Compounds are RESTRICTED USE PESTICIDES (RUP):
RUPs are pesticides that are available for purchase and use only by certified pesticide applicators or persons
under their direct supervision. This is assigned to those products that when used according to directions, are at
a high potential of causing significant human and environmental hazard.
Examples: Diazinon, Fenthion, Methyl Parathion.

15. CARBAMATES
• They are reversible Acetyl cholinesterase inhibitors.
• Examples: Carbaryl (sevin), carbofuran (furadan), methomyl (lannate), propoxur (hit spray), aprocarb (baygon),
aldicarb (temik).
Mechanism of Action:
• Carbamilate the serene moiety of the active site of AChE.
• Reversible reaction.
• They are spontaneously hydrolysed from AChE enzyme site within 48 hours.
• CNS Effects are negligible. ( due to less penetration into CNS).
• Fatal Dose: 10-30 gm ( Carbofuran)
• Fatal period: 2-6 hours(Carbofuran)
So, Less Toxic.

16. SIGNS & SYMPTOMS:
INVESTIGATIONS:
• Blood is drawn to look for presence of poison.
• AChE levels is not reliable, as it comes to normal within hours.
• Same as that of OPC Poisoning.
• Less Prominent CNS Symptoms.

17. TREATMENT:
• Atropine is the Drug Of Choice.
• Oximes – NOT RECOMMENDED.
• However, Oximes can be given during mass casualties, when the type of
insecticidal poison is not known.
• As it is a reversible reaction.
• Also, it may form CARBAMYLATED
OXIMES, which is a much more
potent AChE Inhibitor.
 POST MORETM APPEARENCES: (See Slide No. 12- same as that of OPC).

18. ORGANOCHLORINES
• Chlorinated Hydrocarbons
• Lipophilic– Adipocyte accumulation
• Not considered as first line insecticides
• Remains persistent in environment
• Bioconcentration in food grains
• Carcinogenicity
• Cumulative toxicity
1. Chlorobenzine Derivatives
• DDT , Methoxychlor
2. BHC & Lindane
3. Indane derivatives
• Endrine, Diendrine, Aldrine, Heptachlor,
Chlordane, Endosulphan
4. Chlorinated Camphines
• Toxaphene & Strobane
 ORGANOCHLORINE COMPOUNDS

19. DDT:
• Crystalline powder
• Soluble in mineral & vegetable oils & Organic Solvents.
• Insecticide – Used in WW-II
• Despite worldwide ban, use continued in India.
• Egg thinning in birds.
• Endocrine disruptor in humans
• Moderately Hazardous
• More volatile than DDT
• Accumulates Within Food chain
• Acute Poisoning – Nervous system dysfunction
• Chronic Poisoning– Affect Liver Function
• Banned in many countries
BHC:

20.  ENDRINE:
• Poly chlorinated Hydrocarbon with an INDANE Derivative.
• “Plant Penicillin” – due to wide spectrum of action.
• 3 times more toxic than Aldrin and 15 times more toxic than DDT.
MECHANISM OF ACTION:
• It acts on the Sodium Channels and slows down their closing.
• Sodium conductance across the neuronal membrane of the axon is deranged.
• Causing negative after potential and Hyper-excitability.
• Repeated firing at the nerve membrane.
• Tremors. Acts on the cerebellum and motor cortex of the CNS.
• FIRST STIMULATES, LATER DEPRESSES IT.
• Also, alters the metabolism of Serotonin, Nor- Epinephrine and AcH.

21. • Absorbed from Intact Skin, Inhalation and Ingestion.
• Symptoms start within 15 minutes of ingestion.
• Fatal Dose: 5- 6 gm.
• Fatal Period: 12 to 24 hours. Death occurs within 1 to 2 hours on ingestion of a higher dose.
SYMPTOMS
GIT RESPIRATORY SYSTEM CNS
Nausea, Vomiting, Abdominal
Pain.
Cough, Dyspnoea, Hoarseness
of voice.
Headache, Giddiness,
incoordination, mental
confusion, dilation of pupil,
tremors.
Followed by coma,
convulsions& death due to
Respiratory paralysis.

22. TREATMENT:
• Remove person from source of exposure and remove all clothes.
• Wash the body, prevent cutaneous absorption.
• Gastric lavage.
• Maintenance of patent airway.
• Activated charcoal.
• 5% dextrose solution, if the patient is weak.
• No specific antidote.
• Cholestyramine can be used. it is a bile acid binding resin that can be given orally to increase the fecal excretion of
organochlorines.
POST MORTEM APPEARENCE:
• Froth at mouth and nostrils.
• Air passages contain froth.
• Lungs: Congested and oedematous.
• All internal organs are congested.
• Stomach may contain poison with kerosene like odour, if Aromax is present.
• Brain may be congested and oedematous.

23. MEDICO LEGAL IMPORATANCE of ORGANOCHLORINES.
Suicide Very Common.
Homicide Rare, due to strong smell and bad taste.
Accidental Quite common; Eg. Qatar & Saudi Arabia poisoning tragedy of 1967.
Occupational Exposure- is possible.
Enidrin resists PUTREFACTION.- So detected in the body for sometime after death.
Restriced use OC In India: DDT, Endosulfan, Lindane.

24. PARAQUAT
• Herbicide and weed killer.
• Dipyridinium chloride- sold as ‘Gramoxone’ ; ‘Weedol’.
MECHANISM OF ACTION:
• Undergoes NADPH dependent reduction
• Form free radical which reacts with molecular oxygen.
• Forms superoxide radical
• Disrupts cellular function and structure
• Causes Cellular Death.

25. CLINICAL FEATURES.
• Inhalation & ingestion.
• Distributed to all organs but more concentrated in Kidneys & lungs.
• Toxin is excreted through urine.
• Fatal dose: 3 to 5 gm.
• Fatal period: 1 to 2 days.
SYMPTOMS
GIT LIVER RS CVS RENAL CNS
Corrosion of
Gastric Mucosa
Liver toxicity,
cholestasis & fatty
change.
Cough, dyspnoea,
pulmonary
edema, ARDS
Hypovolemia,
shock, arrhythmia.
Oliguria,
albuminuria, renal
failure.
Coma,
convulsions,
cerebral edema.
Remove all clothes, wash the patient, with soap and water.
Gastric lavage.
• One litre of Aqueous susoension of Clay to absorb Paraquat.
• Followed by 200 ml of 20% Mannitol.
Actiavted charcoal.
Hemoperfusion.
TREATMENT

26. POST MORTEM APPEARANCE.
Corrosion of lips, mouth,
esophagus and stomach.
LIVER: Centrilobular necrosis
and fatty change.
Kidneys: Cortical Pallor, tubular
necrosis.
Lungs: Congested, edematous,
hemorrhagic, weighs more than
1 Kg.

27. MEDICO LEGAL IMPORATNCE OF PARAQUAT
• Suicide Common; Mode of intake is mostly ingestion, but IM and IV injections have also been
reported.
• Accidental Due to its Brown color; resembles cola drinks- so easily ingested.
• Homicidal Possible, but rare.
• Contaminant of
Marijuana
Paraquat has been used to control illegal growth of Cannabis- resulted in contamination of
Marijuana Cigarettes.

28. PYRETHRINS & PYRETHROIDS
• Extracts of plant - Chrysanthemum.
• Less toxic in nature.
• Pyrethroids are synthetic analogues of pyrethrins.
• Insect repellents, insecticides and pesticides.
• Examples: Pyrethrin, allethrin, D Allethrin, Permethrin, Fenvalerate, Sypermethrin.
• Fatal Dose: 1gm per kg weight.
Mechanism of Action: Prolongs inactivation of Sodium channel by binding with it.
INHALATION INGESTION
Rhinorrhea, Sore Throat, wheezing, Dyspnea. Nausea, Vomiting, Vertigo, Fasciculations,
Hyperthermia, Convulsions, Coma.

29. Stomach Wash.
Activated Charcoal.
Wash Skin with Soap & Water to prevent cutaneous absorption.
IV Glucose saline.
Maintain Airway.
Oxygen to be given, if needed.
Signs & Symptoms based on mode of poisoning:
INHALATION INGESTION
Rhinorrhea, Sore Throat, wheezing, Dyspnea. Nausea, Vomiting, Vertigo, Fasciculations,
Hyperthermia, Convulsions, Coma.
 TREATMENT:

30. ZINC PHOSPHIDE.
• Used as rodenticide.
• Grey crystalline powder with garlicky odour.
MECHANISM OF ACTION: Acts by reacting with HCl in the body forming Phosphine which is highly
toxic.
Fatal dose : 5gm.
Fatal period: 24 hrs.
SYMPTOMS
GIT RS CVS CNS RENAL LIVER
• On ingestion
causes
burning
sensation
• Nausea
• Vomitting.
• Dyspnea
• Cyanosis
• Fever
• Respiratory
Distress.
• Dysrhythmias
• Circulatory
collpse.
• Coma
• Convulsions
• Death.
• Renal tubular
necrosis
• Renal failure.
• Hepatic
failure leading
to death

31. Gastric lavage with KMnO4.
Activated charcoal 100g to reduce absorption.
Liquid paraffin for excretion of poison.
IV glucose saline and hydrocortisone.
Oxygen to correct hypoxia.
Na2CO3 for correcting metabolic acidosis.
Hemodialysis for removing poison.
TREATMENT:
• Garlicky smell in the stomach contents.
• All internal organs congested.
• Lungs congested and edematous.
• Fatty change and centrilobular necrosis of liver.
• Brain may be found edematous.
• There may be yellowish discoloration of all
membranes,meninges and costal cartilages.
POST MORTEM
APPEARENCES

32. ALUMINIUM PHOSPHIDE
• Fumigant pesticide and rodenticide.
• Examples: Celphos, Alphos, Quikphos.
• Garlicky odour.
• Aluminium phosphide when on contact with moisture.
• Liberates PHOSPHINE.
• Phosphine is a toxic gas which when absorbed into the system inhibits the
respiratory chain enzymes
• Produces Tissue Anoxia & Necrosis of Liver.
• As it is a systemic poison, it affects all organs of the body.

33. GIT CVS HEPATIC RENAL CNS
Nausea, vomiting,
epigastric pain.
Arrhythmia,
myocarditis,
pericarditis, CCF,
hypotension & shock.
Fatty change,
Hepatitis, Jaundice,
Hepatomegaly, Liver
necrosis, hepatic
encephalopathy.
Renal tubular
necrosis, Renal
failure.
Headache, dizziness,
restlessness,
convulsions, coma
and respiratory
paralysis.
INHALATION
On inhalation, causes Headache, nausea, vomiting,
dizziness, pulmonary edema, respiratory distress,
ARDS, Convulsions, coma.
INGESTION
• On ingestion, Aluminium phosphide reacts with
HCl in the stomach to release phosphine.
• Burning pain, nausea, vomiting, abdominal pain.
• Early symptoms will be less or nil.
• Hepatic and renal failure appears late.
• So, the patient should be kept under observation if
there is a history of poisoning.
 SIGNS & SYMPTOMS:

34. Gastric lavage with 1:10,000 KMnO4 – to oxidise the poison.
Activated charcoal- to absorb the poison.
Antacids- to protect the mucosal layer of stomach.
Liquid paraffin- to increase the excretion from gut.
IV Infusion of glucose saline to correct hypotension & shock.
Hydrocortisone – to reduce Pulmonary edema and respirtory distress.
Oxygen therapy- to correct Hypoxia.
Sodium carbonate- to correct metabolic acidosis.
Magnesium sulphate- To correct hypo magnesemia and arrhythmia. It stabilizes the
free radical stress due to phosphine.
Peritoneal or Hemodialysis- for acute renal failure.
* Should not give STOMACH WASH- Since on contact with it, it releases more
phosphine and this can perforate the stomach.
TREATMENT

35. • Garlic odour from mouth, nostrils and stomach contents.
• Forth +
• Stomach contents, when on contact with water, it will
fumigate.
• Liver: fatty change, centrilobular necrosis on HPE.
• Brain: congested and edematous.
• Adrenals: congested and sometimes, hemorrhagic.
• Kidneys: congested and edematous.
• Heart: Congested; petechial hemorrhages.
• Lungs: Congestion, oedema, Round cell infiltration.
• Liver: Micro Vacuolization, centrilobular necrosis, mononuclear infiltration, fatty
change.
• Kidney: Congestion, RTN.
• Adrenal Glands: Hemorrhagic necrosis.
HISTOPATHOLOGY
POST MORTEM CHANGES

36. CHEMICAL TESTS FOR ALUMINIUM PHOSPHIDE:
Put a paper impregnated with SILVER NITRATE to the gastric aspirate.
Black
Due to presence of phosphine which will convert silver nitrate to silver phosphate.
Gas Chromatography to detect phosphine in blood.
 CIRCUMSTANCES OF POISONING:
• Suicide.
• Accidental- mostly in children.
• Homicidal: rare.
* Its fumigant nature and toxicity makes it a potential agent for CHEMICAL TERRORISM.

37. MEDICO LEGAL IMPORTANCE OF ALUMINIUM
PHOSPHIDE POISONING.
Suicide Very common. (especially in Northern India).
Accidental Occasionally.
Homicidal Rare- due to its smell.
Restricted use Pesticide in India.

38. INORGANIC
PHOSPHOROUS

39. • PHOSPHORUS
WHITE/ YELLOW PHOSPHORUS RED/ AMORPOUS PHOSPHORUS
• Used In Fertilizers, Insecticides, Rodenticides,
Fireworks
• Garlicky odour, garlicky taste, luminosity in the dark.
• On exposure to air, it will burn with yellow fumes-
PHOSPHORESCENCE.
• Formed by heating yellow phosphorus in 240-250
°c.
• No taste/ smell/ luminescence.
• In pure form, it is non toxic.
 COMMERCIAL USES: Making Insecticides, Rodenticides, Fireworks, Fertilizers, Explosives, Incendiary
Bombs.

40. 1. Converted to HYDROPHOSPHORUS and PHOSPHORUS ACID in the body.
Protoplasmic poison, so affects CELLULAR OXIDATION.
TISSUE DESTRUCTION by affecting carbohydrate, protein and fat metabolism.
2. HEPATOTOXIC
Causes fatty degeneration of Liver and Brain.
Mechanism of action:
• Has DIRECT action on Heart and Blood Vessels.
• Skin coming in contact with Yellow Phosphorus- Burns and Blisters.

41. FULMINATING TYPE ACUTE POISONING
• Seen when more than 1 gm is
consumed.
• May die due to CARDIO VASCULAR
COLLAPSE.
• Due to direct action of phosphorus
on heart & blood vessels.
FIRST STAGE SECOND STAGE THIRD STAGE
• On consumption,
burning pain from
mouth to stomach.
• Followed by thirst,
nausea & vomiting.
• Acute gastroenteritis
with Diarrhoea &
Epigastric
discomfort.
• Symptom free.
• Lasts for 2-3 days.
Hepato-Renal
Failure.
Hemetemesis,
Jaundice & Renal
Failure.
Liver is affected
first.- enlarged &
tender.
Hepatic
Encephalopathy.
CNS affected-
Muslcle cramps,
Convulsions,
Priapism, delirium,
Coma.
• CAUSE OF DEATH: Hepatorenal failure or action on CNS and Respiratory failure.
SIGNS & SYMPTOMS

42. • Fatal Dose: 60 to 120 mg.
• Fatal Period: 2 – 8 days.
Gastric lavage using 1:1000 KMnO4- converts phosphorus to phosphoric acid &
phosphates- harmless.
CuSO4- converts phosphorus to copper phosphide- relatively harmless substance.
*not recommended due to risk of Copper Poisoning.
Vitamin K- to correct Hypo thrombinemia.
Activated charcoal.
IV Glucose Saline.
Hemodialysis/ Peritoneal dialysis- if Renal Failure +
OIL/ FAT should not be given, as phosphorus is absorbed into them.
TREATMENT

43. Inflammatory changes in Esophagus and
Stomach.
Luminous material seen in GIT.
Garlic odour to gastric contents.
Liver: Jaundice,fatty change, Centrilobular
steatosis and necrosis.
If the patient survived for more than one
week,
YELLOW ATROPHY of LIVER.
CLOUDY SWELLING of KIDNEYS.
Fat emboli +/-.
PMS: Dark Brown/ Yellow.
POST MORTEM
APPEARENCES

44. MEDICOLEGAL ASPECTS.
SUICIDAL HOMICIDAL ACCIDENTAL
As it is readily available. Rare. May occur in children by licking
the sides of matchboxes.
• Safety matchsticks contain Potassium chlorate, antimony sulphide and powdered glass.
• Striking surface contains red phosphorus, powdered glass and sand.
• Chronic poisoning- industrial hazard.

45. CHRONIC POISONING with PHOSPHORUS.
• Results in PHOSSY JAW. - osteomyelitis of jaw in chronic phosphorus poisoning.
• Frequent inhalation of fumes, may cause necrosis of lower jaw in the region of decayed tooth.
• Common in workers at phosphorus industry, who are exposed to fumes of phosphorus.
• Lesion present as Osteomyelitis occurring in Mandible or maxilla with multiple sinuses, opening
onto external surface, with discharge of foul smelling pus.
• Can result in disfigurement of face.
• Presents with Pain and swelling in Jaw; loosening of teeth.
• Infected bone- glows with green white fluorescence.
PATHOGENESIS:
Phosphorus fumes enter decayed tooth.
Phosphorus enters the jaw through decayed tooth.
Necrosis of tooth and bone.
Osteomyelitis within 2-5 years.

46. • Regular mouthwash by sodium bicarbonate.
• Filling up cavities in mouth. Extraction of decayed tooth.
• Surgical removal of affected bone- to avoid systemic effects, if any.
PROPHYLAXIS:
Proper Ventilation in work place, proper cleansing, sanitation etc.
 TREATMENT:

47. MEDICO LEGAL IMPORATANCE OF PHOSPHORUS.
Long retention in organs after Death:
• Continues to remain in body even after death- unchanged.
• Found upto one month after death- even in exhumed bodies.
Homicide • Rare; due to luminescence & garlicky odour.
Suicide • Deliberate ingestion of Rat Paste.
• Swallowing small crackers; mixing of match heads with alcohol etc.
Accidental • Inadvertent ingestion of Rat Paste.
• Rat paste contains 3% phosphorus.; looks very much like toothpaste, but can be differentiate
by its brown colour, watery consistency and strong unpleasant odour- but can cause
accidental poisoning in children.
Bombs • NAPALM Bombs- Disperses phosphorus on explosion- if alive after attck; the will surely die of
phosphorus poisoning.

48. THE END