When farmers were in search of a cheap, most efficacious and easy to use and freely available pesticide fumigant,they found Aluminium Phosphide(ALP) in 1940.
But the First idiot who tasted it for death was in 1981,since then, the number of cases is progressively increasing throughtout the NorthIndia so much so that it is now the single most suicidal
method and the problem has acquired an epidemic
proportion
Physical Properties:
Chalky white or brown 3 gm. tablets containing 56% of ALP and 44% of ammonium carbonate.
The Way it is being used:
The tablets are taken out of sealed container and placed on stored grains and storage container is closed for few days to combat moles and vermines in granaries.
 |
| celphos were not used as routine pesticide,it is a fumigant. |
Reactions:
ALP has relatively high
vapour pressure that allows it to penetrate porous material
effectively. On coming into contact with water or
moisture or OH radical of air or hydrochloric acid in
stomach,3 gm. tablet of ALP liberates 1gm. of phosphine
or phosphorus hydrogen and each 0.6 gm pellet
0.2 gm of phosphine gas, i.e.,
ALP + 3H20 ----->AL(OH)3 + PH3(in air)
ALP + 3HCL------>ALCL3 + PH3 (in air and stomach)
Few facts about Phosphine (PH3):
PH, is a colourless gas with fishy or garlic odour .
It is removed with half life of 5-24 hours.
The non-toxic residues i.e. phosphites and
hypophosphites of aluminum left in the grains, are less
than 0.1 mg/kg of PH3 for raw cereals, the WHO/FAO
recommended permissible levels regarded safe for human
consumption.
Pathogenesis of toxic effects:
Irrespective of routes of exposure, viz., the
inhalation, ingestion or ocular, the toxic effects of
PH3 are same except initially and are dose dependent.
Some of ALP is directly absorbed from stomach to reach
liver to liberate PH3 slowly to prolong the toxic effects of poisoning.
PH3 is rapidly absorbed from stomach or lungs by
simple diffusion, oxidized slowly.The systemic toxic effects appears in 1-60 minutes after ingestion.This is what the problem of celphos,it reaches and bites the heart soon,so patient will be dying by the time he reaches hospital.
It is excreted in urine as hypophosphite and also excreted unchanged through
lungs significantly.
Basic Act behind the effect:
PH3 inhibits the electron transport resulting from
preferrential inhibition of cytochrome oxidase leading
to respiratory chain inhibition which leads to cellular
hypoxia and small vessel injury which is further
potentiated by cardiotoxicity
due to anoxic myocardial
damage and shock
Direct toxic effect of ALP on myocardium or
hypomagnesemia brought on by focal myocardial
damage leads to arrhythmia s. Hypo tension and shock
ensue within 3-6 hours of ingestion of ALP. In survivors,
the cardiotoxicity and hypoxia disappear within 5-7 days
due to excretion of PH3 and restoration of normal cellular
metabolism.
ECG changes in Celphos poisoning:
The toxic chemical myocarditis leads to
varied fatal ECG changes, 6 to 24 hours after ingestion
in non-survivors, in the form of VE beats, conductionlungs significantly.
Basic Act behind the effect:
PH3 inhibits the electron transport resulting from
preferrential inhibition of cytochrome oxidase leading
to respiratory chain inhibition which leads to cellular
hypoxia and small vessel injury which is further
potentiated by cardiotoxicity
due to anoxic myocardial
damage and shock
Direct toxic effect of ALP on myocardium or
hypomagnesemia brought on by focal myocardial
damage leads to arrhythmia s. Hypo tension and shock
ensue within 3-6 hours of ingestion of ALP. In survivors,
the cardiotoxicity and hypoxia disappear within 5-7 days
due to excretion of PH3 and restoration of normal cellular
metabolism.
ECG changes in Celphos poisoning:
The toxic chemical myocarditis leads to
varied fatal ECG changes, 6 to 24 hours after ingestion
disturbance, LBBB, ventricular fibrillation, aberrant
conduction and idioventricular rhythm terminally leading
to asystole. The non-fatal ECG changes appear
within 12 to 24 hours in survivors and disappear within
56 to 80 hours. Death in first 24 hours appears to be
cardiogenic as evidenced by shock and ECG abnormality.
The serum electrolytes are within normal limits and not
correlated with ECG changes. Since the survivors show
complete normal ECG recovery, it denotes that the effect
of poisoning is due to some reversible factor leading to
disturbance in the permeability of sodium (Na+),
potassium (K+), calcium (Ca2+) and magnesium (Mg2+)
ions leading to change in trans membrane action potential
due to focal myocardial involvement and subsequent
myocardial necrosis, resulting in release of reactive species and intermediates.
within 12 to 24 hours in survivors and disappear within
56 to 80 hours. Death in first 24 hours appears to be
cardiogenic as evidenced by shock and ECG abnormality.
The serum electrolytes are within normal limits and not
correlated with ECG changes. Since the survivors show
complete normal ECG recovery, it denotes that the effect
of poisoning is due to some reversible factor leading to
disturbance in the permeability of sodium (Na+),
potassium (K+), calcium (Ca2+) and magnesium (Mg2+)
ions leading to change in trans membrane action potential
due to focal myocardial involvement and subsequent
myocardial necrosis, resulting in release of reactive species and intermediates.
Chugh et al. has shown that ingestion
leads to high superoxide dismutase activity and low
catalase levels that result in increased formation of free
radicals and accelerated lipid peroxidation. Lipid
peroxidation in turn results in damage to cellular
membrane, disruption of ionic barrier, nucleic acid
damage and cell death
Hypomagenesemia seen in ALP poisoning may be due
to an oxidative stress which buffers the Mg2+ resulting
in increased susceptibility of oxygen free radicals injury
and accerlated lipid peroxidation . High level of SOD
(Superperoxide Dismutase) and MDA (Malonyl
dialdehyde) seen in non-survivors suggests their direct
relation to mortality, whereas the catalase has inverse
relationship. The return of SOD and MDA to normal suggests abolition of an oxidative stress due to elimination of phosphine.
Intractable shock may be due to arrhythmia,
conduction disturbance and myocardial damage. The
peripheral circulatory failure (PCF) due to wide spread
small vessel injury leads to peripheral vasodilatation
leading to shock. Excessive vomiting due to fluid loss
results into shock. Direct toxic effects of PH3 on adrenal
cortex accompanied by decreased cortisol levels, leads
to shock and high mortality .
Injury to alveolar capillary membrane by PH3 while
being inhaled, leads to ARDS (Adult Respiratory Distress
Syndrome) which may also occur rarely if patient has
consumed more than 2 to 3 tablets of ALP.
Wide spread capillary damage leads to bleeding
diathesis, disseminated intravascular coagulation (DIC)
and acute tubular necrosis (ATN).
Shock and DIC lead
to terminal renal failure.
Direct toxic effects of ALP or its adsorbed products
or metabolic acidosis on muscles leads to muscular
ischemia and degeneration of nonspecific nature leading
to myopathy.
In blood, the PH3 changes the circular dichroitic
spectra of hemoglobin and change in haem iron leading
to conformational changes of the prosthetic group.
The blood PH3 levels are positively co-related to the
clinical grades of ALP toxicity and to the dose of the
pesticide consumed . The occurrence of intravascular
hemolysis with ALP poisoning in a patient with normal
G6PD levels is of significance as jaundice in patients
with this poisoning is often attributed to the hepatic
damage alone.
In addition to the effect on the adrenal cortex, ALP
also affects glucose metabolism leading to hypoglycemia,
hyperglycemia or no change effects which can be attributed
to the wide variety of changes in Mg2+, Ca2+, phosphate,
citrate or cortisol levels which act as active stimulatory or
inhibitory modulators to enzymes and hormones that
catalyze and regulate glucose metabolism.
Fatal dose
The specified fatal dose is 0.15-0.5 gm. However, most
of the patients present with ingestion of three or more
tablets which invariably results in death.
Management of celphos poisoning:
As with any other poisoning,the primary aim is to decontaminate the stomach.But in this circumstance,to reduce the absorption of
phosphine, gastric lavage with potassium permanganate
(1:10,000) is done. Permanganate is used as it oxidizes
PH3 to form non-toxic phosphate.
This is followed by a slurry of activated charcoal (approximately 100 gm)
given through a naso gastric tube. A cathartic (liquid
paraffin) is given to accelerate the excretion of
aluminium phosphide and phosphine. Antacids and
proton pump blockers are added for symptomatic
relief
Treatment of Shock
• Intravenous fluids 4 to 6 liters within 3-6 hours
the 50% of which should be normal saline, with
concommitent central venous pressure (CVP)
monitoring to raise it to 10 cm. of H20.
Inj.hydrocortisone 400 mg every 4 to 6 hours is
highly effective to decrease capillary leakage in
lungs in ARDS and to potentiate the
responsiveness of the shock to the endo-or
exogenous catecholamines.
Low dose dopamine (4-6 μg/kg/min) is given to keep
systolic blood pressure >90 mm Hg
Send Out the criminal:
Phosphine excretion can be increased by maintaining
adequate hydration and renal perfusion with
intravenous fluids and low dose (4-6 μg/kg/min)
dopamine. Diuretics like frusemide can be given if
systolic blood pressure is >90 mm Hg to enhance
excretion as the main route of elimination of phosphine
is renal.
Treatment of Cardiac Arrhythmias
MgSo4 is effective in first 24 hours in dose of 1
gm. iv stat after dissolving in 100 ml of 5% dextrose or NS
and 1 gm. every hour for next 3 hours and then 1 gm.
every 6 hours for 5-7 days in continuous iv infusion in
5% dextrose. It corrects cardiac arrhythmias by
modulating sympathetic, parasympathetic and slow
channel kinetics. Mg2+ level should be
maintained at less than toxic levels of 10 meq/l. The
magnesium level achieved with said dosage schedule is
2.00 to 3.1 meq/I.
The conventional antiarrhythmic drugs, viz;
digoxin and xylocaine are not effective and cardioversion
is not attempted due to diffuse myocarditis
Metabolic Acidosis
Bicarbonate level less than 15 mEq/L requires sodabicarb in a dose of 50-100 mEq intravenously every 8 hour till the bicarbonate level rises to 18-20 mEq/L. Patients may
require up to 300-500 ml of sodium bicarbonate. The peritoneal or haemodialysis is useful in case, if metabolic acidosis persists in haemodynamically stable patients.
leads to high superoxide dismutase activity and low
catalase levels that result in increased formation of free
radicals and accelerated lipid peroxidation. Lipid
peroxidation in turn results in damage to cellular
membrane, disruption of ionic barrier, nucleic acid
damage and cell death
Hypomagenesemia seen in ALP poisoning may be due
to an oxidative stress which buffers the Mg2+ resulting
in increased susceptibility of oxygen free radicals injury
and accerlated lipid peroxidation . High level of SOD
(Superperoxide Dismutase) and MDA (Malonyl
dialdehyde) seen in non-survivors suggests their direct
relation to mortality, whereas the catalase has inverse
relationship. The return of SOD and MDA to normal suggests abolition of an oxidative stress due to elimination of phosphine.
Intractable shock may be due to arrhythmia,
conduction disturbance and myocardial damage. The
peripheral circulatory failure (PCF) due to wide spread
small vessel injury leads to peripheral vasodilatation
leading to shock. Excessive vomiting due to fluid loss
results into shock. Direct toxic effects of PH3 on adrenal
cortex accompanied by decreased cortisol levels, leads
to shock and high mortality .
Injury to alveolar capillary membrane by PH3 while
being inhaled, leads to ARDS (Adult Respiratory Distress
Syndrome) which may also occur rarely if patient has
consumed more than 2 to 3 tablets of ALP.
Wide spread capillary damage leads to bleeding
diathesis, disseminated intravascular coagulation (DIC)
and acute tubular necrosis (ATN).
Shock and DIC lead
to terminal renal failure.
Direct toxic effects of ALP or its adsorbed products
or metabolic acidosis on muscles leads to muscular
ischemia and degeneration of nonspecific nature leading
to myopathy.
In blood, the PH3 changes the circular dichroitic
spectra of hemoglobin and change in haem iron leading
to conformational changes of the prosthetic group.
The blood PH3 levels are positively co-related to the
clinical grades of ALP toxicity and to the dose of the
pesticide consumed . The occurrence of intravascular
hemolysis with ALP poisoning in a patient with normal
G6PD levels is of significance as jaundice in patients
with this poisoning is often attributed to the hepatic
damage alone.
In addition to the effect on the adrenal cortex, ALP
also affects glucose metabolism leading to hypoglycemia,
hyperglycemia or no change effects which can be attributed
to the wide variety of changes in Mg2+, Ca2+, phosphate,
citrate or cortisol levels which act as active stimulatory or
inhibitory modulators to enzymes and hormones that
catalyze and regulate glucose metabolism.
Fatal dose
The specified fatal dose is 0.15-0.5 gm. However, most
of the patients present with ingestion of three or more
tablets which invariably results in death.
Management of celphos poisoning:
As with any other poisoning,the primary aim is to decontaminate the stomach.But in this circumstance,to reduce the absorption of
phosphine, gastric lavage with potassium permanganate
(1:10,000) is done. Permanganate is used as it oxidizes
PH3 to form non-toxic phosphate.
This is followed by a slurry of activated charcoal (approximately 100 gm)
given through a naso gastric tube. A cathartic (liquid
paraffin) is given to accelerate the excretion of
aluminium phosphide and phosphine. Antacids and
proton pump blockers are added for symptomatic
relief
Treatment of Shock
• Intravenous fluids 4 to 6 liters within 3-6 hours
the 50% of which should be normal saline, with
concommitent central venous pressure (CVP)
monitoring to raise it to 10 cm. of H20.
Inj.hydrocortisone 400 mg every 4 to 6 hours is
highly effective to decrease capillary leakage in
lungs in ARDS and to potentiate the
responsiveness of the shock to the endo-or
exogenous catecholamines.
Low dose dopamine (4-6 μg/kg/min) is given to keep
systolic blood pressure >90 mm Hg
Send Out the criminal:
Phosphine excretion can be increased by maintaining
adequate hydration and renal perfusion with
intravenous fluids and low dose (4-6 μg/kg/min)
dopamine. Diuretics like frusemide can be given if
systolic blood pressure is >90 mm Hg to enhance
excretion as the main route of elimination of phosphine
is renal.
Treatment of Cardiac Arrhythmias
MgSo4 is effective in first 24 hours in dose of 1
gm. iv stat after dissolving in 100 ml of 5% dextrose or NS
and 1 gm. every hour for next 3 hours and then 1 gm.
every 6 hours for 5-7 days in continuous iv infusion in
5% dextrose. It corrects cardiac arrhythmias by
modulating sympathetic, parasympathetic and slow
channel kinetics. Mg2+ level should be
maintained at less than toxic levels of 10 meq/l. The
magnesium level achieved with said dosage schedule is
2.00 to 3.1 meq/I.
The conventional antiarrhythmic drugs, viz;
digoxin and xylocaine are not effective and cardioversion
is not attempted due to diffuse myocarditis
Metabolic Acidosis
Bicarbonate level less than 15 mEq/L requires sodabicarb in a dose of 50-100 mEq intravenously every 8 hour till the bicarbonate level rises to 18-20 mEq/L. Patients may
require up to 300-500 ml of sodium bicarbonate. The peritoneal or haemodialysis is useful in case, if metabolic acidosis persists in haemodynamically stable patients.
N-acetyl cysteine has also been tried in celphos poisoningto reduce oxidative stress.
The average time interval between intake of poison and death is three hours with a range of 1-48 hours, 95% of the patients
die within 24 hours and the commonest cause of death
in this group is arrhythmia. Death after 24 hours is
due to shock, acidosis, ARDS and arrhythmia
The average time interval between intake of poison and death is three hours with a range of 1-48 hours, 95% of the patients
die within 24 hours and the commonest cause of death
in this group is arrhythmia. Death after 24 hours is
due to shock, acidosis, ARDS and arrhythmia
0 comments:
Post a Comment