Pesticides

Synthetic organic insecticides Cholinesterase inhibitors Botanic insecticides Synthetic organic Rodenticides
insecticides
Organochlorine
ORGANOPHOSPHATE INSECTICIDES CARBAMATE INSECTICIDES PYRETHRINS AND e.g. DDT and PHOSPHIDES ANTICOAGULANTS
PYRETHROIDS toxaphene (WARFARIN &
SUPERWARFARIN)
Mechanism of • Inhibition of cholinesterase enzyme in the nervous system Similar to organophosphates except • Mammals are generally 1- Local corrosive • Phosphides liberate phosphine gas • Anticoagulants inhibit
toxicity: resulting in accumulation for: able to metabolize these reaction upon contact with moisture and this vitamin K cycle thus prevent
of acetylcholine thus causing initial stimulation that is followed • Inhibition of cholinesterase is compounds rapidly and 2- Production of reaction is normal blood coagulation.
by depression of reversible within 24-48 hours, so thereby highly reactive free enhanced in the acidity of the stomach. • The anticoagulant effect of
impulse transmission at the following sites: manifestations are less severe and of render them harmless. radical leading to • Phosphine is then absorbed through warfarin is delayed at least 15
1. Postganglionic parasympathetic nerve endings. shorter duration. • Toxicity is primarily lipid per oxidation the GI and respiratory tracts. hours till depletion of
2. Autonomic ganglia and neuromuscular junctions. • Poor penetration of BBB leading to associated with and tissue • Phosphine is a highly toxic gas, existing vitamin K stores and
3. Central nervous system. mild or no CNS manifestations. hypersensitivity destruction that especially to the lungs, brain, kidneys, active coagulation factors.
• Hydrocarbon pneumonitis can occur with aspiration of • Cholinesterase levels are not reactions and direct start with pulmonary heart, and liver
organophosphates dissolved suitable in confirming the diagnosis of irritant fibrosis ending with through inhibition of cytochrome c
in petroleum distillates. carbamate effects. multiple organ oxidase enzyme and free radical
poisoning. failure production.
Clinical • History of exposure (but may not be available). • Anaphylactic reactions ● Organochlorine: Manifestations of systemic toxicity • Single ingestion: of warfarin-
manifestations: • Manifestations usually occur 1-2 hours after exposure but including bronchospasm, - Affect nerve usually appear rapidly after exposure containing rodenticides pose
may be within minutes (inhalation) or may be delayed up to oropharyngeal edema impulse transmission • GIT toxicity: nausea, vomiting, diarrhea no threat to either normal
several hours (skin exposure) with garlic-like odor. and shock (a rotten fish or garlicky odor), or anticoagulated patients.
1- Muscarinic manifestations (DUMBELS) may occur in -Myocardial pancreatitis and hepatitis.
• Diarrhea (defecation) and colic. hypersensitive irritability& • Multiple ingestions:
• Urination. individuals. arrhythmia. • Cardiac toxicity: hypotension potentially produce
• Miosis and blurred vision. unresponsive to pressors, arrhythmias coagulopathy and bleeding
• Bradycardia and hypotension. • With large ingestions, -Hydrocarbon and pericardial effusions. manifested with
• Bronchospasm, wheezing and cyanosis. the central nervous pneumonitis. bruising, hematuria and
• Lacrimation. system may be affected • Respiratory toxicity: pulmonary edema menorrhagia.
• Emesis and nausea. seizures, coma -Hepatic and renal and pleural effusions.
• All secretions are increased (Sweating, Salivation, …) or respiratory arrest. injury Complications:
2- Nicotinic manifestations • Renal toxicity: acute renal failure. Intracranial hemorrhage is
-due to effect on autonomic ganglia & neuromuscular junctions. rare but life-threatening
Hypertension, tachycardia (happen in severe poisoning) and • CNS toxicity: seizures and coma. complication.
mydriasis.
• Skeletal muscle fasciculation, weakness, paralysis and • Metabolic changes: metabolic acidosis,
respiratory arrest. or mixed metabolic acidosis and
• Muscle Cramps and twitchesing respiratory alkalosis are frequent.
3- CNS manifestations
• Anxiety, insomnia, confusion, ataxia, coma. • Disseminated intravascular
• Cheyne-stockes respiration and respiratory and circulatory coagulation, hepatic necrosis and renal
depression. failure may occur.
4- Hydrocarbon pneumonitis
Causes of death: • There is conflicting evidence on the
1- Respiratory failure due to bronchospasm and bronchorrhea occurrence of magnesium disturbances
(due to incease
secretions &drawing inside himself)
2- Circulatory collapse, pancreatitis or cardiac arrhythmia.
Management:
 1-Ensure a patent airway.
2-Obtain 2 intravenous access
3-Place the patient in the left lateral position, ideally in a head-
down position, to reduce the risk of aspiration.

Investigations: 1- Laboratory: Pyrethrins are naturally 1- Laboratory: Prothrombin time (PT), partial
• Cholinesterase level is helpful when diagnosis is not evident, occurring insecticides. • ABG thromboplastin time (PTT),
but it may not be • ▲ Cardiac enzymes. thrombin time, and
immediately available, thus its utility is not in directing acute Pyrethroids are • ▲BUN and serum creatinine fibrinogen
intervention but synthetic derivatives. • ▲ Liver transaminases concentration are used to
in diagnosis and follow up. evaluate the patient.
• ABG, Blood sugar, Amylase, CBC, Liver function tests. 2- ECG: may show arrhythmia & ST-T
wave changes.
2- ECG: may reveal sinus tachycardia or sinus bradycardia, A-V
block, or asystole. 3- Radiology: Chest X-ray may show
pulmonary edema and pleural effusions.
3- Radiology:
Chest X-ray should be examined for evidence of:
• Hydrocarbon aspiration pneumonitis (as some
organophosphates are packaged in a hydrocarbon vehicle).
-Non-cardiogenic pulmonary edema and hyperlucency
consistent with
bronchospasm and air trapping.
Treatment 1- Emergency and supportive measures: Oximes are not indicated as action of • Emergency and 1- Emergency and supportive care: 1- Emergency and supportive
• Airway and breathing management with frequent suctioning carbamate is reversible. supportive care and • Management of shock and institution measures:
of secretions and decontamination of supportive measures as soon as including whole blood
respiratory support is the first priority. Intubation may be Oximes are only allowed in the measures as usual. possible transfusion.
required to facilitate following cases: are the corner stone for treatment and
control of secretions and for ventilatory support if respiratory 1. If the diagnosis is not definite should be provided as required. Life-threatening hemorrhage
failure ensues. weather organophosphates or • Airway and breathing management. is reversed by fresh frozen
• Ventricular arrhythmia, seizures, hydrocarbon pneumonitis, carbamates. • Establish intravenous access and fluids plasma which is rich in
fluid loss and other 2. If it is a case of mixed are given guided by central venous active vitamin K-dependent
manifestations should be controlled as usual. organophosphate and carbamate pressure (CVP). The aim is to keep the coagulation factors.
• Observe asymptomatic patients for 8-12 hours to rule out poisoning. CVP at around 12- 14 cm of water.
delayed-onset • Low dose dopamine can be given to
symptoms especially after skin exposure. -oximes are contraindicated: keep systolic blood pressure >90 mm Hg.
1-it is ineffective to carbamate • Hydrocortisone 200-400 mg IV every 4-
poisoning as in that case the anionic 6 hours can be given to combat shock.
site of the enzyme is • Control ventricular arrhythmia,
not free. seizures and metabolic acidosis.
2-It is rather contraindicated because • The use of magnesium sulphate is still a
it hass weak anti-ChE activity of its matter of conflict.
own.
2- Decontamination: 2- Decontamination: 2- Decontamination:
• Gastrointestinal decontamination: • Caregivers are at risk for secondary Single- or multiple-dose
- It is better not to use ipecac. contamination as exposure to phosphine activated charcoal and/or oral
- Gastric lavage in case of recent ingestion. gas may occur if the patient vomits or if cholestyramine.
- Activated charcoal is administered. gastric lavage fluid is not isolated.
• Dermal decontamination: • Consider gastric lavage with sodium
- Rescuers should wear protective clothing and gloves. bicarbonate has been proposed (to
- Removal of clothes and shoes of the victims. reduce
- Washing the patient’s skin and hair by soap and water. stomach acid and resulting production of
• Eye decontamination: with copious water or saline. phosphine).
• Administer activated charcoal orally if
conditions are appropriate.

• Some studies proposed that, the use of

liquid vegetable oils as coconut oil
prevent liberation of phosphine gas.
3- Antidotes: There is no physiological 3- Enhanced elimination: has no role. 3-
• Atropine: antidote and no need for 4- Antidotes: no specific antidote. Physiological antidotes:
- It reverses only the muscarinic effects. enhancement of vitamin K1
- It is given, after the patient is well oxygenated elimination.
- Dose: 1-2 mg IV repeated until dryness of bronchial secretions.
- After that, atropine should be tapered over the following 24
hours before being discontinued.
● Target end-points for atropine therapy:
1- Clear chest on auscultation with no wheeze.
2-Heart rate >80 beats/min.
3-systolic blood pressure >80 mmHg.
4- Dry axillae.
5-Pupils no longer pinpoint
•Oximes:
-Mechanism of action:
- They reactivate the cholinesterase enzyme.
- Detoxify the organophosphate molecules and they have also
an anticholinergic effect.
- They are most effective when taken early (within 24 hours)
before aging of the cholinesterase enzyme has occurred.
- Pralidoxime
1-2 grams in 100 ml saline to be taken over 30 minutes IV. If no
improvement of muscle power, repeat the dose after 1 hour
and in severe cases, the dose can be repeated every 8-12 hours
till the patient is clinically well.

Phosphides

• Aluminum and zinc phosphides are highly effective insecticides and rodenticides.

• Aluminum phoshide has a higher mortality rate than zinc phosphide.

• They are widely used to protect grains.

• Acute poisoning may be direct due to ingestion of the salts or indirect from accidental inhalation of phosphine gas.

• Phosphides are a leading cause of fatal suicides in developing countries.