(Irritant Inorganic Non Metal Poison)

Dr. Sandip B. Patil

HOD & Professor
DEPARTMENT OF AGADTANTRA
Shree RMD Ayurved College, Valsad
 It exists in 2 forms – White or Yellow and Red or Violet
1) White or Yellow Phosphorus :
 Is highly poisonous, Crystalline, Waxy, Translucent,
 soluble in organic solvents, has garlicky smell,
 is luminous in dark(phosphorescence),
 Ignites at 30 Degree centigrade, becomes yellow emits
fumes of phosphorus trioxide (P2O3) on exposure to air.
 It is stored under water or Kerosene. It is used in chemicals,
fertilizers, rodenticides, fire work and gun powder.
 It should never be touched with fingers.
2) Red or Violet phosphorus :
 It is granular with no taste or smell,
non-poisonous, Non-luminous.
 Mixed with glass, red phosphorus is used on the sides of
match box. (The match stick has Potassium chlorate and
Antimony sulphide)
 MECHANISM OF ACTION :
1) In acute poisoning :- Acts as protoplasmic poison.
 It causes hepatic dysfunction (Hepatotoxicity) resembling
ischaemia – known as Necrobiosis. This results in
disturbance in carbohydrate and fat metabolism.
- Inhibition of deposition of glycogen.
- Increased deposition of fat.
2) In chronic poisoning :- There is excessive bone
formation at the epiphyseal end leading to necrosis and
sequestration.
3) Phosphine gas (PH3) leads to mainly respiratory
manifestations.

 ACUTE POISONING :
 Signs and Symptoms :
Stage I - First latent period of 1-6hrs.
Stage II - GIT and CNS manifestations.
Stage III - Second latent period of 2-3 days.
Stage IV – Liver failure and CNS manifestations.
 GIT manifestations :
▪ Garlicky smell and taste, Burning pain in upper GIT,
▪ Breath and vomitus are luminescent in dark.
▪ Dehydration results. Faint fumes may emanate from stool –
smoky stool syndrome.
 CNS manifestations :
▪ Headache, Insomnia, Deafness, Impaired vision,
▪ Tremors, Convulsion, Paralysis and coma.
 Priapism : Painful persistent erection of penis.
 After 2-3 days ( Hepatic failure) :
▪ Jaundice, pruritis, hepato-spleenomegaly,
▪ distended tender abdomen, abortion, bleeding
through all orifices,
▪ hypoglycaemia, hypoprothrombinemia,
▪ dehydration, electrolyte imbalance,
▪ oliguria, albuminuria and haematuria.
▪ Blisters on the skin and sub cutaneous haemorrhages.
▪ In early stages liver is enlarged due to fatty
degeneration (Necrobiosis) and in later stages it is
shrunken due to necrosis (acute yellow atrophy).
 Cause of Death : Hepatic, Renal or Cardiac insufficiency.
 Fatal Dose :- 100 – 150 mg.
 Fatal period :- Variable
 Treatment :-
 Demulscents are contraindicated because they dissolve
phosphorus.
 Stomach wash, I.V. fluids and glucose for shock and
dehydration.
 Vit K, B-Complex and Vit C, Morphine for Pain.
 Antidote : 0.1% Copper sulphate solution. (Forms non
toxic copper phosphide) or 0.1% Potassium permanganate
(Oxidises phosphorus to phosphoric acid phosphate)
 Even H2O2 and charcoal are useful.
 CHRONIC POISONING :
 It is normally due to exposure to fumes, in people working
in industries where phosphorus is used. It leads to necrosis
and sequestration of bones.
 Signs & Symptoms :
 Weakness, Pain in abdomen, Jaundice, Bronchitis, Pain in
joints, Pain in teeth, Phossy jaw.

 PHOSSY JAW/GLASS JAW :

 It is the manifestation in teeth of chronic Phosphorus
poisoning, resulting due to necrosis and sequestration of
the jaws due to increased bone formation.
 Changes start in the area of a decayed tooth.
Sequestration of necrotic
cortical bone (white)
that is surrounded by reactive
bone (involucrum).
 It is characterised by,
- Pain in teeth.
- Swelling and necrosis of jaw,
especially lower jaw.
- Loosening of teeth.
- Failure of dental socket to heal when teeth fall,
- Inflammation of oral mucous membrane showing small
reddish areas.
- Finally osteomyelitis and necrosis of the jaw occurs with
multiple sinuses discharging foul smelling pus.
- Other Symptoms are Nausea, Vomiting, Anorexia, Pain in
abdomen, Bronchitis, jaundice, Anaemia, Loss of weight,
Pain in joints, Spontaneous fracture may occur.
 Treatment/Prevention includes :
 Use of exhaust fans.
 Regular dental checkups.
 Carious teeth should be filled in or extracted.
 Regular mouth washes with sodium biocarbonate.
 Periodic X-ray examinations of jaws.
 Cause of death – are Infection, Pyemia and weakness due
to dysphagia.
 POST-MORTEM APPEARANCE :
 I) In early deaths : Skin is yellow and shows sub
coetaneous haemorrhages.
 Inflammations, erosions and some time perforations of
upper GIT,
 Stomach contents luminous and garlicky,
 Cloudy degeneration of liver and kidney.
 Liver is enlarged, friable and haemorrhagic.
 II) In late deaths : Jaundice, Bleeding from orifices,
dehydration, bleeding from internal organs, liver
degeneration,
 Liver is small, Leathery and dirty yellow.
 MEDICOLEGAL ASPECTS :
 1) Derivatives of phosphorus are Phosphoric acid,
Phosphine, Aluminium phosphide and Zinc phosphide.
 2) Is used for suicide, homicide and to cause criminal
abortion.
 3) Used in insecticides, rodenticides and fire-arm
ammunition.
 4) To set fire and to create smoke-screens.
 Moist cow dung mixed with yellow phosphorus is wrapped
in wet cloth and thrown on thatched roof.
 Same way it can be put in letterbox to destroy undesired
letters.
(Corrosive vegetable acid poison)
 The group is known as cyanogen/Prussic acid. It is
chemically HCN. Other cyanides are Potassium
cyanide KCN and Sodium cyanide NaCN.
 It is one of the strongest poisons known.
 The group is known as Vegetable acid since
hydrocyanic acid is present in certain fruits -plum,
peach, pear, apple, apricot, cherry and bitter almonds,
as glycoside 'Amygdalin', which is harmless
(Amygdaline is combination of glucose, benzaldehyde
and cyanide).
 Cyanides are also used in Chemistry laboratory, gold
plating, fertiliser industry and for fumigation of ships,
railway carriages etc.
 PHYSICAL CHARACTERISTICS :
 HCN (hydrogen cyanide) is normally in the form of
colourless gas with smell like bitter almonds, liquid
form is hydrocyanic/prussic acid and KCN is a dirty
white powder, while NaCN is yellowish.
 MECHANISM OF ACTION :
 Cyanides act as protoplasmic poisons by inhibiting the
enzyme cytochrome oxidase (chelation of ferric
component of cytochrome), thereby converting
pyruvate to lactate thus reducing oxygen utilisation in
the cells resulting in cytotoxic hypoxia. Since the tissue
respiration stops, death in cyanides is immediate.
 Death is by bulbar paralysis.
BULBAR PALSY :
SIGNS AND SYMPTOMS:
 Poisoning results on ingestion, inhalation and
absorption through abraded skin.
 With large doses, sudden death can occur. With low
doses, giddiness, nausea, headache, confusion,
dyspnoea, cyanosis, fine froth at nose and mouth,
convulsions and dilated pupils. Sometimes clenched
teeth is seen. Breath smells of bitter almonds.
 Inhalation of vapours of hydrocyanic acid results in
feeling of constriction in chest, throat, dizziness,
vertigo, insensibility and death.
 Potassium cyanide which is strongly alkaline, causes
corrosion of upper GIT, epigastric pain, vomiting,
 cyanosis, oronasal froth, dilatation of pupils,
imperceptible pulse, shallow respiration, coma and
death.
FATAL DOSE:
 For HCN - 60 mg or 1 : 500 concentration
 In air For KCN - 200 mg.
FATAL PERIOD :
 Usually death is immediate though sometimes it may
be delayed by 2-10 min.
 Contrary to popular belief, there is a time gap between
onset and termination.
TREATMENT :
 Treatment has to be immediate
 Object and principle of treatment : It is to avoid
cyanogen - cytochrome combination and principle of
treatment involves the conversion of Hb to meth Hb
 Meth Hb with cyanides forms cynmeth Hb (harmless).
Sodium thiosulphate given I.V. combines with cyanide
to form Sodium thiocyanate which is excreted by
kidney.
 Nitrites convert haemoglobin to meth haemoglobin.
 Meth Hb+CN =Cyn meth Hb (harmless)
 Na2S203 +CN = Sodium thiocyanate (excreted by
kidney)
 I) 3 ampoules of 0.2 ml Amyl nitrite are broken in
handkerchief and given for inhalation. (stop if systolic
B.P. falls below 80)
+
10 ml of 3% Sodium nitrite given IV.
+
 50 ml of 25% Sodium thiosulphate Na2S203 (hypo)

 II) Co2EDTA, or dicobalt edetate i.e. Dicobalt tetra

acemate (Kelocyanor) 600 mg I.V. followed by 20ml of
50% glucose I.V. (Dicobalt edetate acts as chelating
agent and forms inert complexes - Cobaltocyanides
and Cobalticyanides).
III) Other compounds which are useful in cyanide poisoning
are :
- Dimethylaminophenol (DMAP)
- Methylene blue
- PAPP (Para aminopropiophenone)
- Cobalt acetate
- Saturated glucose solution
 (These compounds also convert Hb to Meth Hb).
IV) Hydroxocobalamin can also be used
 - with cyanides it forms cyanocobalamin i.e., Vit. B-12.
V) In case of consumption of low doses - emetics are given
and gastric lavage (with 25% Hypo) is done, after specific
treatment.
VI) In case of inhalation of cyanide, artificial respiration,
oxygenation and coramine are given.
POST MORTEM APPEARANCE :
1) Cyanosis
2) Froth at nose and mouth
3) Pink post mortem lividity
4) Smell of bitter almonds from the stomach contents
and body tissues.
5) Slight corrosion
6) Features of asphyxia.
MEDICOLEGAL ASPECTS :
1) KCN itself is not poisonous. It combines with gastric Hcl
acid to form HCN acid which causes toxic effects.
KCN+Hcl = HCN +Kcl
In case of absence of gastric Hcl i.e. achlorhydria like in
pernicious anaemia no poisoning occurs due to KCN (it is
doubtful).
MEDICOLEGAL ASPECTS :
2) In places where it is available, it is commonly used for
suicide.
3) It is sometimes used for homicide and as cattle
poison.
 Gassing with cyanide in the camp of Hitler during 2nd
world war killed thousands of Jews.
4) Cyanide gas is used in gas chamber to kill the
condemned prisoner in UK.
5) Accidental poisoning in laboratories and industries is
common.
6) Usually terrorists keep cyanide capsules and commit
suicide when caught.
Cyanide Capsules :