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Rodenticides are a heterogeneous group of
compounds that exhibit markedly different
toxicities to humans and rodents. They are
among the most toxic substances regularly
found in homes.
Types of Rodenticides
Metal phosphides :
• Zinc phosphide
• Aluminum phosphide
Others as thallium,yellow phosphorus and arsenic.
25 years old male patient came to Ain shams
poison control Centre with history of black fine
powdered rodenticide ingestion from 2hrs , he
was vitally stable and clinically free and emesis
was done to him by using sodium bicarbonate and
the patient admitted in the hospital.
1hr later the patient complained from vomiting
and epigastric pain , investigations were done
(ECG , ABG and liver functions) alls are normal
except pH was 7.20 and bicarbonate was
11 mmol/l .
Then the patient transferred to ICU for correction of
metabolic acidosis .
6 hrs later the patient became very irritable and the
liver functions test show elevated liver enzymes .
4 hrs later the patient suffered from flapping tremors
and disturbed conscious level .
What was this rodenticide ?
Zinc phosphide is an inorganic
compound that combines phosphorus
with zinc. It is a black powder used in
rodenticide baits. with a characteristic
3 Zn + 2 P → Zn3P2
How does zinc phosphide work?
When zinc phosphide is eaten by either an animal or
a person, stomach acid causes it to release the toxic
The phosphine in the stomach then crosses into the
body's cells, and stops the cells from producing
energy by Inhibition of cytochrome oxidase enzyme
leading to inhibition of aerobic metabolism that
leads to lactic acidosis and cell death.
Zinc phosphide affects all cells, but targets cells in
the heart, lungs, and liver.
Its main effect is metabolic acidosis, hepatotoxicity
and cardio toxicity.
There are documented cases of adults dying from
massive doses of the Zinc Phosphide (4 g to 5 g)
although others have survived acute exposure of as
high as 25 g of zinc phosphide if vomiting occurred
early and pre exposure to moisture.
Irritability and restlessness are the earliest symptoms
Vomiting ,diarrhea and dehydration.
hypotension , chest tightness, coldness,
unconsciousness and coma .
Toxic cardiomyopathy with dysrhythmia.
Sever toxic hepatitis .
Death can occur from pulmonary oedema and liver
History and clinical picture
investigations: ECG , ABG and liver functions.
Elimination: emesis or GL is done using NaHCO3.
IV fluids and electrolytes to correct electrolyte
inotropics and antiarrhythmic for toxic myocarditis .
In 2008"After fully assessing human health and
ecological effects, as well as benefits The US
Environmental Protection Agency made restriction
to the use of zinc phosphide.
It is classified as a federally restricted use pesticide
because of its hazard to non target species and its
acute toxicity to humans.
But in Egypt it is still used with easy availability
in homes !!!!!!
الغلة اصرأق –السوس سم
Powdered Aluminium (Al) and Red Phosphorus (P)
reacts with each other and produces Alp. Present in the
form of tablets each is about 3gm, grey in colour and has
a smell that resembles that of garlic or rotting fish.
Aluminium Phosphide Applications
It can be used as:
Aluminium phosphide poisoning is wide
spread in various parts of the world especially
in developing countries where it is extensively
used as a highly toxic, low cost rodenticide and
grain preservative .
Because of its easy availability in the household
it has become an important means of self
Trade names: Quickphos, cellphos and
Mechanism of action
Upon exposure to moisture, water and air it liberates
phosphine gas, which is absorbed rapidly by inhalation
and gastro intestinally.
The phosphine in the stomach then crosses into the
body's cells, and stops the cells from producing energy
by Inhibition of cytochrome oxidase enzyme, leads to
lactic acidosis and cell death.
a fatal dose is between 150mg and 500mg.
The mortality rates from ALP vary from 45–80%. The
actual numbers of cases may be much larger, as less
than 5% of those with ALP eventually reach a tertiary
It has been reported to be the most common cause of
suicidal death in India.
Other reported cases in Egypt , Nepal, new zeland,
Saudi Arabia, Morocco and Tehran.
Aluminium phosphide poisoning is systemic and it
affects various organ systems like the cardiovascular,
gastrointestinal, renal ,respiratory and hepatobiliary
include epigastric discomfort, nausea, and vomiting
and burning sensation in stomach.
The cardiovascular involvement :
take the form of myocarditis, peripheral circulatory
failure, arrhythmias or cardiac failure. Electro-cardio
graphic abnormalities include ST-T wave changes,
supra ventricular tachycardia with conduction
defect, atrial fibrillation, bundle branch block and
Nervous system involvement:
occurs in the form of headache, paraesthesia,
dizziness and tremors.
majority of patients come in shock with
impalpable pulse, cold extremities, restlessness,
palpitation and tachypnea.
Occasionally cases may come with picture of adult
respiratory distress syndrome (ARDS), pulmonary
oedema, acute renal failure and peripheral
circulatory failure often leading to death which is
The diagnosis is based on reliable history and or
the production of remaining tablets empty
container by the attendants of the patient for
identification. Patient’s breath has garlic like smell
Further confirmation can be made by subjecting
the gastric lavage fluid to silver nitrate test,this test
is based on the property of PH3 to reduce silver
nitrate to metallic silver which appears black to the
There is no known antidote to aluminium
phosphide and management of the patient is
mainly supportive in order to sustain life till
phosphine is excreted from the body by lungs and
There is controversy about the use of magnesium
sulphate but then magnesium sulfate is used
because of its anti-arrhythmic action. Intravenous
magnesium sulphate (a loading dose of 4 gm. over
4 hours followed by 1 gm. I/V 6 hourly) and
Calcium gluconate is beneficial because of its
cardio protective action.
Successful treatment of acute aluminium phosphide
In the Poison control Centre, Loghman-Hakim
Hospital, University of Medical Sciences Tehran,
A medical staff members said that they used the
following protocol in a 28-years old man who had
ingested a lethal amount (12 g) of aluminum
phosphide with suicidal intent and was admitted to
hospital approximately 6 hours post ingestion. The
patient had signs and symptoms of severe toxicity,
and his clinical course included metabolic acidosis
and liver dysfunction.
Treatment consisted of gastric lavage with
potassium permanganate solution, intravenous
administration of sodium bicarbonate,
magnesium sulphate and calcium gluconate, and
oral administration of coconut oil
as rapid prevention of absorption by coconut oil
might be helpful.
Conservative and supportive therapy in the
Intensive Care Unit was also provided. The
patient survived following rapid treatment and
It is concluded that coconut oil has
a positive clinical significance and
can be added to the treatment
protocol of acute aluminum
phosphide poisoning .