Toxicology Animals Poisons copy-FINALUNIT2.pptx

bvssudaynadh116fsctoxicology
Forensic Toxicology
TOXICOLOGY OF
ANIMAL POISONING
Unit II

SCORPIONS
• Belong to Arthropods
• All of them are poisonous & their venoms are more
potent than that of snakes & numerically more than
snakes, so they represent more public health problems,
especially in southern areas
• Generally, more dangerous & causing more morbidity &
mortality in children.
Ex: Androctonus Amoreuxi

Scorpion Venom
• Generally more toxic, more variability of specific toxins & more
multiplicity of antigens than snake venom
• Consists of amino acids, peptides & small proteins (mainly
neurotoxin, nephrotoxin, cardiotoxin, hemolytic toxin, histamine,
serotonin, anti-ACh-esterase) & enzymes such as phospholipases,
hyaluronidases, phosphodiesterase.
• Injectable LD: few up to 50 μ g
• Humans have unique variable susceptibility to scorpion venom

Toxic Mechanism of Scorpion Venom
• Neurotoxin:
• Block voltage-gated Na+ & Ca++ channels….prolonged action potential &
excessive release of catecholamine…..adrenergic manifestations
• The long-chain polypeptide neurotoxin causes stabilization of voltage-
dependent sodium channels in the open position, leading to continuous,
prolonged, repetitive firing of the somatic, sympathetic, and parasympathetic
neurons. This repetitive firing results in autonomic and neuromuscular over-
excitation symptoms, and it prevents normal nerve impulse transmissions

• The short polypeptide neurotoxin blocks the potassium channels.
• Anti-cholinesterase….. accumulation of Ach…..cholinergic
manifestations…….this will lead to marked CV effects
• Autonomic excitation leads to cardiopulmonary effects observed after
some scorpion envenomations.
• Somatic and cranial nerve hyperactivity results from neuromuscular
overstimulation.
• Serotonin may be found in scorpion venom and is thought to
contribute to the pain associated with scorpion envenomation.
• A smaller child, a lower body weight, and a larger ratio of venom to
body weight lead to a more severe reaction

Factors Affecting Severity of Scorpion Sting
• Age & body size of the victim
• Species & size of scorpion
• The amount of venom injected
• Site & number of stings
• Individual susceptibility to venom

Clinical Manifestations
• Local: Severe Intense Pain, Edema, Numbness & Tenderness.
• CVS: Sinus Arrhythmias (Abnormal ECG), Hypertension, Pulmonary
Edema, Ischemic Changes in ECG (Condition in which the heart does
not receive enough amount of blood and oxygen), Complications Are
More In Children With Increased LDH (Lactate Dehydrogenase) &
CPK (Creatine Phosphokinase).
• CNS : Agitation, Paresthesia (Tingling, Burning, Pricking Or
Prickling, Skin-crawling, Itching), Irritability & (Restlessness, Severe
Involuntary Shaking &Jerking Extremity Due To Somatic Skeletal
Neuromuscular Dysfunction). Cerebral Edema -> Convulsions & Coma
• Others: Nausea & Vomiting, Hypothermia, Blurring Of Vision, Tongue
Fasciculation Slurred Speech, Diaphoresis, Tearing

Management of Scorpion Venom
• First aid: like a snake but, it is mandatory to control local pain (use local anesthesia)
to make the patient calm which is a very important procedure in the management
• Specific treatment: use polyantivenom as in snake
• Supportive treatment:
- Wash the wound with a Weak Ammonia, Borax, or Potassium Permanganate
solution.
- Symptomatic treatment: Haloperidol controls agitation (State of Neuroexcitation).
- Calcium gluconate is given through IV to control local Swelling.
- Use Diazepam (Type of Benzodiazepines) in convulsions.
- Use Diuretics (Drugs used to increase the flow of urine) in pulmonary edema which
helps in removal of excess water than normal.

• Don't attempt to cut the wound and suck out the poison. This can
cause infection or transfer the venom into the bloodstream of the
person attempting to remove the poison.
• Scorpions cannot usually deliver enough venom to kill a healthy adult.
While venom toxicity varies among species, some scorpions contain
very powerful neurotoxins, which, ounce for ounce, are more toxic to
humans than the venom of cobras.
• However, scorpions inject relatively small amounts of venom
(compared to snakes), so the overall dose of toxins per sting is
survivable.

Black widow spider
• Belong to Arthropods
• Only female bites is clinically significant
• Identified by a red to orange hour-glass on the thorax
• Contains a potent neurotoxin that destroys cholinergic
nerve terminals with a massive release of A Ch
especially at motor end plates causing severe muscle
spasms & also, affecting adrenergic nerve terminals
that may cause an increase in sympathetic outflow

Clinical Manifestations
• Local: Bite is usually painless & local reaction is very rare in the form
of pain, redness, edema & itching
• Systemic: Develops 1-3 hours ranging from mild affection to serious
troubles & mostly in the form of severe muscle spasms leading to chest
& abdominal pain.
• There will be a circulatory collapse, convulsions, and Delirium (Serious
mental abilities) which may be confused with Tetanus and strychnine
poisoning.
• Tremors (a neurological condition that includes shaking or trembling
movements in one or more parts of the body, most commonly affecting a
person's hands) & muscle fasciculation (individual Muscle twitching)
followed by muscle weakness – hypertension – nausea, vomiting &
salivation

Management of Spider Bite
• IV Calcium Gluconate which controls pain and abdominal cramps &
considered an antidote.
• Latrodectus antivenin
• Diazepam
• Methocarbamol (Relieve Muscle Cramps)
• Opioid analgesics
• The antivenin is reserved for patients with severe cramps.
• Dapsone - 50 to 100 mg twice daily for 2-3 days.

To be continued……..
With Heavy metal Poisoning

INORGANIC
Metallic and Non- Metallic

What’s In
• Introduction to Heavy metals
• Signs and Symptoms
• Route of Exposure and Mode of Action
• Fatal Dose and Fatal Period
• Treatment
• Postmortem Appearance

Introduction
Arsenic (As)
• Physical Properties: Greyish metal, brittle, and has a metallic luster.
• Chemical Properties: Atomic number 33, commonly found in
compounds such as arsenic trioxide.
• Molecular Weight: 74.92 g/mol
• Atomic Number: 33
Lead (Pb)
• Physical Properties: Dense, malleable, bluish-white metal that tarnishes
to a dull grey.
• Chemical Properties: Atomic number 82, often found in lead oxide.
• Atomic Number: 82 bvssudaynadh116fsctoxicology

Mercury (Hg)
• Physical Properties: Silvery liquid metal at room temperature.
• Chemical Properties: Atomic number 80, forms various
compounds like mercury chloride.
Cadmium (Cd)
• Physical Properties: Soft, bluish-white metal that is ductile
and malleable.
• Chemical Properties: Atomic number 48, often found in
cadmium sulfide.

Toxic Forms
Arsenic
• Arsenic Trioxide (As2O3): One of the most toxic forms, often
used in chemotherapy. It is a white, odorless solid that can
cause severe poisoning.
• Arsenate (As5+): Less toxic than arsenites but still harmful. It
can mimic phosphate in biological systems, disrupting cellular
functions.
• Toxicity Mechanism: Arsenic inhibits key metabolic
processes, particularly affecting mitochondrial function and
energy production, leading to multi-organ damage by tissue
edema and hemorrhage.
• Exposure Routes: Ingestion of contaminated water or food,
inhalation of dust or fumes, and dermal contact with arsenic-
treated materials.

Lead
• Lead Acetate:- ‘SUGAR OF LEAD’ A soluble form of
lead that can cause acute poisoning.
• Lead Oxide (PbO): Common in industrial settings like
storage batteries, solders, Paints, Hair Dyes, and Electric
cables and can lead to chronic exposure toxicity.
• Toxicity Mechanism: Lead disrupts enzyme function
which is responsible for Heam synthesis, interferes with
neurotransmitter release, and causes oxidative stress,
particularly affecting the nervous system.
• Exposure Routes: Ingestion of lead-contaminated food
or water, inhalation of lead dust (often in occupational
settings), and dermal exposure from lead-based paints.

Mercury
• Methylmercury: A highly toxic organic form that
bioaccumulates in fish and seafood, leading to severe
neurological damage upon consumption.
• Mercuric Chloride (HgCl2): An inorganic form that is highly
toxic and can cause acute gastrointestinal and renal damage.
• Other forms include mercuric oxide, mercuric cyanide,
mercuric sulfide (Cinnabar, Sindoor), and mercuric sulfate.
• Toxicity Mechanism: Mercury disrupts cellular processes,
particularly affecting the cerebellum, nervous system, and
kidneys. It can lead to protein denaturation and oxidative stress.
• Exposure Routes: Inhalation of mercury vapor (common in
industrial settings), ingestion of contaminated fish, and dermal
exposure to mercury-containing products.

Signs and Symptoms
Arsenic Poisoning
Types of Symptoms:
1. Severe abdominal pain, vomiting, diarrhea (often bloody), shock, and Peripheral
Vascular failure.
2. GI form is most common type of Acute Poisoning and which resembles Bacterial
Food Poisoning.
3. Intense Thirst and stools were filled with blood and dark in colour and later
becomes colourless & watery which resembles “RICE WATER STOOLS OF
CHOLERA”
4. Symptoms can escalate to GARLICKY ORDOUR BREATH
5. CVS: Acute circulatory collapse and tachycardia, etc.
6. CNS: Headache, Vertigo, General Paralysis, Peripheral Neuropathy, convolutions
and Coma.
7. Delayed Symptoms like Hair loss, Skin eruptions, and death may occur due to
circulatory failure.

Difference between Arsenic Poisoning and Cholera

• SKIN:- Rain Drop Pigmentation is one of the characteristic Symptoms of Chronic
arsenic Poisoning which may persist for months.
• Aldrich-Mees- Mees Lines on the Nails is also one of the characteristic Symptoms of
Arsenic Poisoning in prolonged contact.
• Watery eyes and Photophobia are also seen.
• Chronic Nephritis and Bone Marrow Suppression, May lead to Leukemia and skin
cancer as Arsenic is TERATOGENIC ( Can cause Birth defects).
• Narcotic Form – Tenderness in Muscles, delirium, coma, and Death, and GI symptoms
are very Slight.
Rain Drop Pigmentation Aldrich-Mees- Mees Lines
Rain Drop Pigmentation Aldrich-Mees- Mees Lines

Mercury Poisoning
• Symptoms
• Muscle weakness, poor coordination, numbness in the hands and feet,
skin rashes, anxiety, memory problems, trouble speaking, hearing, or
seeing
• High-level exposure
• Known as Minamata disease; in children, it can result
in acrodynia (pink disease) where the skin becomes pink and peels
• Long-term complications
• Kidney problems and decreased intelligence

First Phase Symptoms
• The initial phase of mercury poisoning often includes breathing
difficulties, such as shortness of breath or cough.
• Metallic taste: A distinct metallic flavor in the mouth.
• Color changes: Skin discoloration, particularly pink cheeks and extremities,
the mouth tongue, and faucets become corroded and swollen and show
greyish-White coating.
• Gastrointestinal symptoms: Nausea, vomiting, abdominal pain, and blood-
stained diarrhoea.
• The vomit Contains greyish slimy mucoid material with blood and Shreds of
mucus membrane.
• These symptoms can arise quickly, especially with elemental mercury
exposure through inhalation or spills.
• Neurological symptoms: Tremors, irritability, mood swings, and sleep
disturbances.
• Inhalation of fumes may lead to serious nervous symptoms like ataxia
(Collectiveness disorder that affects coordination, balance, and speech),
restriction of the visual field, and delirium.
Color changes in Tongue

Second Phase Symptoms
• As mercury levels increase, the following symptoms may
develop if the person survives the first phase: Which
generally starts in 1-3 days.
• Glossitis and Ulcerative Gingivitis appear within 24-36 hrs.
Which is followed by the loss of teeth and necrosis of Jaw
may occur.
• Acute ulceration of colonic mucosa can be seen.
• Muscle weakness: Difficulty in coordination and strength.
• Peripheral neuropathy: Numbness or tingling in
extremities.
• Cognitive impairments: Memory problems, difficulty
concentrating, and emotional instability.
• Kidney damage: Potential for renal failure in severe cases
and renal tubules may show necrosis.
Ulcerative Gingivitis
Acute ulceration of
colonic mucosa

Normal and Chronic Exposure Levels
•Normal blood mercury levels: Typically less than <10 µg/L.
•Normal urine mercury levels: Generally below <20 µg/L.
Chronic Exposure Levels
•Chronic blood mercury levels: Can exceed >30 µg/L, often leading
to neurological and renal complications.
•Chronic urine mercury levels: Levels above >150 µg/L may
indicate significant exposure and potential toxicity

Specific Conditions Related to Mercury
Poisoning
• Hydrargyrism (Advanced Conditions)
• Hydrargyrism, or mercury poisoning, can lead to
severe neurological and physical symptoms,
including Hatter's Shakes: (MAD HATTER’S
DISEASE) Characterized by tremors and
emotional disturbances.
• Mercurial Erethism: A condition involving
irritability, depression, and other psychological
symptoms due to mercury exposure.
• Mercurial Lentis: Ocular symptoms including
vision changes and potential blindness due to
mercury toxicity.

Acrodynia (Pink Disease)
Acrodynia, also known as pink disease,
primarily affects children and is characterized
by:
•Skin changes: Bright pink coloration of the
hands, feet, and nose.
•Other symptoms: Peeling skin, irritability,
and lethargy. This condition was historically
linked to mercury in teething powders

Minamata Disease
• Minamata disease is a severe form of mercury poisoning resulting from industrial
discharge into water bodies, leading to methylmercury accumulation in fish.
• The tragedy highlighted the health impacts of mercury exposure, particularly among
local populations reliant on contaminated fish from Minamata Bay in Japan in 1956.
• Signs and Symptoms of Minamata Disease: Neurological symptoms such as tremors
and ataxia.
• Cognitive impairments and sensory disturbances.
• Severe cases can lead to coma and death

Lead Poisoning
• Signs and Symptoms:
• An Astringent and Metallic Tase, dry through, thirst, burning abdominal
pain, nausea, vomiting, sometimes diarrhoea, peripheral circulatory
collapse, headache, insomnia, depression, coma, and death.
• Cerebellar ataxia is common in children with acute lead Poisoning.
• Plumbism; Saturnism is caused by acute poisoning of lead.
• Caused due to inhalation of lead dust and fumes by the markers of white
lead marker and users of lead paints (Most commonly in children).
• Lead vapor is more dangerous than lead dust.

• Facial pallor (Pale colouration) especially at the mouth is
one of the Earliest signs.
• Basophilic Stippling is also one of the characteristic
symptoms that is usually seen in red blood cells.
• Stippled red cells may also seen in arsenic and zinc
Poisoning.
• Eosinophilia is more common than Basophilic Stippling
• Lead Palsy usually occurs late and is most common in
Adults which affects muscle weakness and may lead to
wrist and foot drops.
Basophilic Stippling
in red blood cells
Wrist And Foot Drops.

• Lead Lines- A Stripped Blue Line called a Burtonian Line is a characteristic
symptom usually seen in 50-70% of cases.
• Lead Encephalopathy is seen almost all cases of Plumbism usually In children
and is associated with tetrahedral lead.
• Lead encephalopathy occurs in high whole-blood lead levels over 80 to 100
μg/dL. At such concentrations, lead crosses the blood-brain barrier and
ultimately leads to the breakdown of cerebrovascular endothelium, causing
increased capillary leak and edema.
• Other symptoms like general weakness, irritability, foul breath, headache,
vertigo, loss of hair and drowsiness
Burtonian Line

Diagnosis
• Usually diagnosed by blood tests and Other
historical symptoms.
• X- Ray will show the radio-opaque Bonds or
lines at the metaphysis of long bones and
Long with the margins of the iliac crest is
seen in children.
• X-ray may show Radio-Opaque substance in
the GI tract if lead is ingested in 36-48 hrs.
Radio-opaque Bonds Or Lines

Post Mortem Appearance
• Arsenic Poisoning:
• External Appearance
• Eyeballs: The eyeballs may appear sunken and dehydrated due to
fluid loss during the putrefaction stage.
• Skin: The skin often shows signs of dehydration, resulting in
wrinkling and discoloration.

• Internal Appearance
• Stomach: During the putrefaction stage, yellow streaks can be observed in the
subperitoneal layer of the stomach and, to a lesser extent, the intestines. This
phenomenon occurs due to absorbed arsenic being converted into sulfide.
• Liver: The liver may appear enlarged and congested. There may be patchy fatty
degeneration and jaundice present, indicating damage from arsenic exposure.
• Heart: The heart may exhibit petechial hemorrhages under the endocardium,
particularly in the left ventricle. The myocardium can show signs of degeneration,
and there may be evidence of myocardial damage due to toxic effects.
• Chronic Gastritis: Prolonged exposure to arsenic can lead to chronic gastritis,
characterized by inflammation and irritation of the stomach lining.
• Kidney: Due to the toxic effects of arsenic, the kidneys may show signs of
damage, such as congestion and inflammation.

Chronic Gastritis Pectineal Hemorrhages in Heart

Treatment:
1.Stomach Wash: If arsenic ingestion is recent, gastric lavage (stomach wash) with water or
a dilute bicarbonate solution may be performed to remove unabsorbed arsenic.
Antidotes:
• Dimercaprol [British Anti-Lewisite (BAL)]: A chelating agent (A chemical compound
that binds tightly to metal ions) that binds to arsenic and facilitates its
excretion from the body.
• Succimer (DMSA): An oral chelating agent used for treating arsenic poisoning,
particularly effective in children. (2,3-dimercapto-1-propanesulfonic acid)Penicillamine:
Another chelating agent that can be used in cases of arsenic poisoning.
• Supportive Care: This includes intravenous fluids, electrolyte replacement, and
monitoring for complications such as shock or kidney failure.
• Hemodialysis: In severe cases, hemodialysis may remove arsenic from the bloodstream.
• Vitamin and Mineral Supplementation: Supplementing with antioxidants like vitamin C
and E may help mitigate some toxic effects.

• Mercury Poisoning:
• Tongue: Is white and sodden in appearance, and the mouth generally has a
diffuse grayish-white escharotic appearance. Mucous membranes of the
alimentary tract are inflamed and corroded. The muscular coats are softened,
so that removing an organ causes its entire rupture.
• Kidneys: show toxic nephritis, Renal damage, particularly tubular nephritis.
• Liver: Shows cloudy swelling or fatty degeneration, Fatty degeneration of
liver and cardiac muscle.
• Subendocardial hemorrhages are present in the heart.
• Drastic changes in the large intestine, with spreading necrosis, which may
even involve the whole of the large intestine (Intestinal ulceration).

• Treatment:
• Immediate Care: Decontamination: Remove any contaminated clothing and wash
the skin thoroughly with soap and water to prevent further absorption.
• Supportive Care: Provide intravenous fluids to maintain hydration and electrolyte
balance.
• Gastric Lavage: If ingestion occurred recently, gastric lavage may be performed to
remove unabsorbed mercury from the stomach. (2-5% Sodium Bicarbonate may used
for Gastric Lavage to bind the Mercury).
• Penicillamine is used for less severe Mercury vapor and Inorganic Mercury poisoning
(Orally 1g/day for 5 days)
• Chelation Therapy: Dimercaprol (BAL): Administered intramuscularly; it binds to
mercury and facilitates its excretion through urine.
• Symptomatic Treatment: Manage symptoms such as nausea, vomiting, and diarrhea,
and Hemodialysis is required if any significant kidney damage.

• Lead Poisoning:
• Signs of acute Gastroenteritis are seen.
• The stomach’s mucosa may be thickened and softened with the eroded
patches and covered with greyish-white deposits.
• Kidneys: Chronic lead exposure often leads to nephropathy, characterized
by tubular damage and interstitial fibrosis.
• Liver: Hepatic damage may be observed, although it is less common.
• Brain: In cases of severe poisoning, cerebral edema, and degeneration can
occur, particularly affecting the cortex.
• To be precise the brain appears to be very pale in color and gently swollen.

• Hematological Changes:
• Anemia: Lead interferes with hemoglobin synthesis, leading to
microcytic anemia. This may be evident in post-mortem blood
analyses.
• Basophilic Stippling: This is a specific finding in red blood cells due
to the inhibition of enzymes involved in heme synthesis.
• Gastrointestinal Tract:
• Lead Colic: Post-mortem examinations may reveal signs of colonic
spasm or inflammation due to lead toxicity.
• Skeletal Changes:
• Lead Lines: Radiologically, lead lines may be visible on bones,
indicating chronic exposure.

Treatment
• Treatment strategies vary based on the severity of poisoning and the
presence of symptoms such as encephalopathy.
• Chelation Therapy
• Chelation therapy is essential in treating lead poisoning. It involves
using chelating agents that bind to lead, facilitating its excretion from the
body through urine.
• Dimercaprol (BAL): Administered intramuscularly; typically used for
severe cases.
• Calcium Disodium EDTA (CaNa2 EDTA): Administered
intravenously or intramuscularly; effective for moderate to severe
poisoning.
• D-Penicillamine: An oral chelating agent used for chronic lead
poisoning; dosage varies based on individual needs.

Dosage Guidelines
Severe Poisoning (without encephalopathy):
• BAL: 3–5 mg/kg IM every 4 hours for 2 days, then every 12 hours for up to
10 days.
• CaNa2 EDTA: 50 mg/kg/day IV or IM divided into two doses for 5 days if the
Lead-blood level is >70µg/100 ml of blood.
• Moderate Poisoning:
• CaNa2 EDTA (Edetate Calcium Disodium): Same as above but may consider
shorter treatment duration based on clinical response.
Mild Poisoning:
• D-Penicillamine: Initial dose of 30 mg/kg/day in 3 divided doses, increasing
as tolerated up to a maximum of 1 g/day.
• Succimer (DMSA): Can Also be used at 10 mg/kg/dose twice in a day for 20
days.

Non-Metallic Poisons

Inorganic Irritant Poisons
• Inorganic irritant poisons are harmful substances that can cause
significant tissue damage upon exposure. Notable examples
include:
1. Phosphorus
• Toxic Forms: White Phosphorus (P4) is highly toxic and can
cause severe systemic effects, while Red Phosphorus is less
toxic and primarily associated with methamphetamine
production.
2. Iodine
• Toxic Forms: Elemental iodine and iodides can irritate mucous
membranes and cause thyroid dysfunction at high doses.
3. Chlorine
• Toxic Forms: Chlorine gas (Cl2) is a potent respiratory irritant,
causing damage to the lungs and mucous membranes.

Phosphorus Poisoning (P4)
Signs and Symptoms
• Phosphorus poisoning can be categorized into three stages
based on the timing of symptoms following exposure.
• Fulminating Poisoning
• Occurs with ingestion of more than 1 gram of white
phosphorus.
• Symptoms may include: Severe cardiovascular collapse
• Shock
• Death may occur within 12 hours due to direct cardiac
toxicity and Blood vessels.
• Thirst, Severe Nausea and Vomiting occur.

Acute Poisoning
• Acute poisoning is characterized by three distinct stages:
1. First Stage (Hours of Exposure)
• Symptoms appear within hours of exposure: Nausea, vomiting,
diarrhea, and severe abdominal pain.
• Breath and excreta have a Garlic-like Odor.
• Diagnostic features include Luminescent Vomit and Feces due to
the spontaneous combustion of phosphorus in air.
2. Second Stage (Symptom-Free Period)
• Lasts for approximately 2-3 days: Patients may appear symptom-
free, but liver enzyme levels rise, indicating hepatic injury.

3. Third Stage (Systemic Toxicity)
• Begins after the symptom-free period: Systemic symptoms include:
Nausea, vomiting, diarrhoea, hematemesis (vomiting blood).
• Hepatomegaly (liver enlargement), tenderness, jaundice, Pruritus
(itchiness).
• CNS symptoms such as Convulsions, Delirium, and Coma.
• Potential causes of death include: Shock
• Hepatic failure
• CNS damage
• Renal insufficiency

Difference between White Phosphorus and Red Phosphorus

Iodine Poisoning
• Iodine poisoning occurs due to excessive exposure to iodine, particularly in
its elemental form or concentrated solutions. Understanding its physical
properties, toxic forms, and mode of action is essential for recognizing and
managing this type of poisoning.
Physical Properties of Iodine
• Chemical Formula: I2
• Appearance: Violet-black crystals with a metallic sheen.
• Melting Point: 113.7 °C (236.7 °F)
• Boiling Point: 184.3 °C (363.7 °F)
• Density: 4.944 g/cm³
• Solubility: Sparingly soluble in water but readily soluble in organic
solvents like alcohol and ether.

Toxic Forms
• Iodine is toxic in its elemental form (I2) and can be found in various
compounds, including iodides and iodophors (e.g., povidone-iodine).
Concentrated solutions of iodine are particularly corrosive.
Mode of Action
• Iodine acts primarily as a protoplasmic poison, affecting cellular functions like
• Protein Binding: Iodine binds to proteins, disrupting cellular metabolism and
leading to necrosis.
• Corrosive Effects: The vapours irritate the respiratory passages, potentially
causing Pulmonary edema and Glottic edema (Laryngeal edema-fluid
accumulation up in the tissues surrounding the larynx) upon exposure.
• Gastrointestinal Damage: Ingestion leads to severe irritation and necrosis of
the gastrointestinal tract.

Signs and Symptoms of Iodine Poisoning
General Symptoms
1.Iodine poisoning manifests through various signs and symptoms, which can be
classified into immediate corrosive effects and systemic reactions:
2.Corrosive Effects: Burning sensation and pain in the mouth, throat, and
stomach.
3.Intense thirst, excessive salivation, and vomiting.
4.Lips and angles of the mouth may be stained brown from iodine contact.
5.Vomiting Characteristics: Vomited matter may appear Dark Yellow or Blue,
especially if starch is present.
6.Excreta may also exhibit a peculiar iodine odor.
7.Urinary Changes: Urine may be scanty or suppressed, presenting a Red-
Brown Color with albumin.

8. Metabolic Effects: Metabolic acidosis may occur alongside nephritis
and renal failure.
9. Cardiovascular Symptoms: Pulse rate may be slow and weak;
hypotension can develop.
10. Dermatological Reactions: Skin may become cold and clammy,
with possible rashes.
Specific Complications
• Respiratory Distress: Glottic and Pulmonary edema can lead to
asphyxia.
• Shock: Severe cases may result in shock due to fluid loss from
vomiting and diarrhea.

Phosphorus Poisoning
• Fatal Dose: 60-120 mg of phosphorus can be lethal.
• Fatal Period: Death may occur within 2 to 8 days following exposure.
Post-Mortem Appearances of Phosphorus Poisoning
• In cases of phosphorus poisoning, post-mortem examinations reveal distinct signs of tissue damage
and systemic effects on the esophagus and Stomach; irritation may be evident, with the presence of
luminous material found in the stomach.
• In acute poisoning, the gastric and intestinal contents may emit a garlic-like odor and display
luminescence.
• Mucous Membranes: These membranes may appear yellowish or greyish-white, exhibiting
destroyed patches.
• Multiple smaller or larger hemorrhages can be observed.
• Liver: The liver becomes swollen, yellow, soft, and fatty, making it easily ruptured. Acute yellow
atrophy (rare Kidney disorder) is often present.
• Kidneys: Kidneys may show yellow discoloration along with some hemorrhages.
• Heart: The heart appears flabby and demonstrates fatty degeneration.
• Blood: Blood is often tarry with diminished coagulability.

• Chronic Poisoning
• Chronic phosphorus poisoning typically results
from prolonged exposure, often through
inhalation of fumes over several years. This
condition can lead to “Phossy Jaw”
Characterized by necrosis of the lower jaw and
decayed teeth due to the corrosive effects of
phosphorus vapors.
• This condition is medically termed osteomyelitis,
which refers to inflammation of the bone or bone
marrow usually caused by infection.
• Symptoms of Phossy Jaw: Necrosis leads to
multiple sinuses that discharge foul-smelling pus.
Phossy Jaw

• Circumstances of Poisoning
• Phosphorus poisoning can occur under various circumstances:
• Accidental Exposure: Often occurs through fireworks or
rodenticides.
• Homicidal Intent: Occasionally used in deliberate poisoning cases.
• Alcohol Mixtures: Phosphorus may be mixed with alcohol for
nefarious purposes.

Post-Mortem Appearances of Iodine Poisoning
• Acute Poisoning
• In cases of acute iodine poisoning, post-mortem examinations reveal
distinct pathological changes in various organs:
• Gastrointestinal Tract: The mucosa of the stomach and intestines
is inflamed and excoriated, often appearing brown due to the corrosive
effects of iodine.
• Heart, Liver, and Kidneys: These organs typically show signs
of fatty degeneration, indicating cellular damage and metabolic
disturbances.
• Brain: There may be edema of the brain, contributing to increased
intracranial pressure.

Chronic Poisoning (Iodism)
• Chronic iodine poisoning, known as iodism, manifests with a
variety of symptoms affecting multiple systems:
Symptoms of Iodism:
• Pain over the sinuses
• Rhinorrhea (running nose)
• Conjunctivitis (inflammation of the eye)
• Increased salivation
• Nausea and vomiting
• Emaciation (weight loss)
• Lymphadenopathy (swelling of lymph nodes)
• Parotid swelling (often referred to as "iodide mumps")
• Wasting of breasts and testes
• Skin manifestations such as acne or Erythematous patches
Iodide Mumps
Erythematous patches

Treatment for Phosphorus Poisoning
• The treatment of phosphorus poisoning involves several critical steps aimed at
decontamination, supportive care, and addressing specific complications. Here’s a
detailed overview of the treatment protocols:
1. Gastric Lavage
• Potassium Permanganate Solution: Gastric lavage can be performed using a
potassium permanganate solution, which oxidizes phosphorus to phosphoric acid and
phosphates, rendering it harmless.
• Activated Charcoal: Administering activated charcoal can help absorb the poison,
reducing its systemic absorption.
2. Copper Sulfate Solution
• The stomach may be washed with a 0.2% copper sulfate solution or 0.2 g of copper
sulfate may be given every minute until vomiting occurs. This treatment coats the
phosphorus particles with a film of copper phosphide, which is relatively harmless.

3. Vitamin K Administration
• To combat hypoprothrombinaemia (a deficiency of prothrombin leading to
bleeding), Vitamin K can be administered in 20 mg via IV, repeated as necessary.
• Blood Transfusion: In cases of severe bleeding or significant coagulopathy, a blood
transfusion may be required. Blood transfusion is the process of transferring blood or
blood products into a person's circulation to replace lost components.
4. Avoidance of Oils and Fats
• Oils and fats should be avoided as they dissolve phosphorus and promote its
absorption into the body.
5. Hemodialysis
• Hemodialysis is preferred in cases of severe renal failure or significant metabolic
derangements, as it helps remove toxins from the bloodstream.
6. Management of Burns
• If burns occur due to phosphorus exposure, they should be thoroughly washed with
a 1% copper sulfate solution in water to prevent further tissue damage.

Treatment for Iodine Poisoning
• The management of iodine poisoning involves several decontamination and
supportive measures aimed at mitigating the toxic effects of iodine. Here’s a
comprehensive overview of the treatment protocols:
1. Emetics and Gastric Lavage
• Emetics: Inducing vomiting can help expel the ingested iodine from the stomach.
• Gastric Lavage: The stomach may be washed out with warm water containing
soluble starch and albumin, which can help bind iodine and facilitate its removal.
2. Sodium Thiosulfate
• A 1-5% solution of sodium thiosulfate can be administered. This solution converts
the tincture of iodine to harmless iodide, effectively neutralizing its toxic effects.
3. Sodium Chloride
• Administering sodium chloride promotes the excretion of iodide by competing
with iodide at the level of renal tubules, thereby reducing its harmful effects.

4. Alkaline Solutions
• Alkalis, such as barley water or arrowroot, can be given to help
neutralize stomach acidity and provide symptomatic relief.
5. Activated Charcoal
• Activated charcoal can be administered to bind iodine in the
gastrointestinal tract, preventing further absorption into the bloodstream.
6. Treatment of Skin Lesions
• Skin lesions resulting from iodine exposure can be treated with a 20%
alcohol solution, which helps to disinfect and soothe affected areas.
7. Symptomatic Treatment
• Supportive care should include monitoring vital signs and treating
symptoms such as nausea, vomiting, and abdominal pain

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