Poisoning - Pesticides in Children - Clinicals, Diagnosis, and Management

Pediatric emergencies

Clinicals - History

Fact Explanation
Anxiety, seizures ,headache, dizziness Organophosphates inhibit cholinesterase leading to excess acetylcholine (Ach). Carbamates reversibly inhibits cholinesterase.
Overstimulation of nicotinic acetylcholine receptors in the central nervous system (CNS), due to accumulation of ACh leads to these symptoms.
Organoclorines induce hyperexcitable state in central and peripheral nervous system by disruption of normal flow of sodium and potassium across the axon membrane,it may antagonize GABA-mediated inhibition in CNS giving rise to these symptoms
Anxiety, seizures ,headache, dizziness
Organophosphates inhibit cholinesterase leading to excess acetylcholine (Ach). Carbamates reversibly inhibits cholinesterase.
Overstimulation of nicotinic acetylcholine receptors in the central nervous system (CNS), due to accumulation of ACh leads to these symptoms.
Organoclorines induce hyperexcitable state in central and peripheral nervous system by disruption of normal flow of sodium and potassium across the axon membrane,it may antagonize GABA-mediated inhibition in CNS giving rise to these symptoms
Muscle twitching, muscle weakness Nicotinic effects due to excess acetylcholine Muscle twitching, muscle weakness
Nicotinic effects due to excess acetylcholine
sweating, salivation, diarrhea, tearing Muscarinic effects due to excess acetylcholine sweating, salivation, diarrhea, tearing
Muscarinic effects due to excess acetylcholine
Breathing difficulty Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh leads to depression of respiration.
Excess acetylcholine at muscarinic acetylcholine receptors causes wheezing due to broncho constriction
Breathing difficulty
Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh leads to depression of respiration.
Excess acetylcholine at muscarinic acetylcholine receptors causes wheezing due to broncho constriction
Unconscious Due to coma caused by depression of respiration and circulation ( Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh ) Unconscious
Due to coma caused by depression of respiration and circulation ( Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh )

Clinicals - Examination

Fact Explanation
Hypertension When there is an accumulation of acetylcholine (ACh) at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system Hypertension
When there is an accumulation of acetylcholine (ACh) at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system
Bradycardia Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh leads to depression of circulation Bradycardia
Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh leads to depression of circulation
Convulsions Overstimulation of nicotinic acetylcholine receptors in the central nervous system (CNS), due to accumulation of ACh.
Organoclorines induce hyperexcitable state in central and peripheral nervous system
Convulsions
Overstimulation of nicotinic acetylcholine receptors in the central nervous system (CNS), due to accumulation of ACh.
Organoclorines induce hyperexcitable state in central and peripheral nervous system
Miosis Effects of organophosphate poisoning on muscarinic receptors (excess acetylcholine) Miosis
Effects of organophosphate poisoning on muscarinic receptors (excess acetylcholine)
Dyspnea , ronchi Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh leads to depression of respiration.
Excess acetylcholine at muscarinic acetylcholine receptors causes wheezing due to broncho constriction
Dyspnea , ronchi
Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh leads to depression of respiration.
Excess acetylcholine at muscarinic acetylcholine receptors causes wheezing due to broncho constriction

Investigations - Diagnosis

Fact Explanation
Plasma choline esterase levels / levels of OP metabolites Organophosphates (OP) Inhibit cholinesterase.
Measurements of OP metabolites in both the blood and urine can be used to determine if a person has been exposed to organophosphates. Specifically in the blood, metabolites of cholinesterases, such as butyrylcholinesterase (BuChE) activity in plasma, neuropathy target esterase (NTE) in lymphocytes, and of acetylcholinesterase (AChE) activity in red blood cells
Plasma choline esterase levels / levels of OP metabolites
Organophosphates (OP) Inhibit cholinesterase.
Measurements of OP metabolites in both the blood and urine can be used to determine if a person has been exposed to organophosphates. Specifically in the blood, metabolites of cholinesterases, such as butyrylcholinesterase (BuChE) activity in plasma, neuropathy target esterase (NTE) in lymphocytes, and of acetylcholinesterase (AChE) activity in red blood cells

Investigations - Management

Fact Explanation
Tendon reflexes can be decreased or absent due to muscle weakness caused by intermediate syndrome which can occur between 24-96 hours (1-4 days) after organophosphate poisoning Tendon reflexes
can be decreased or absent due to muscle weakness caused by intermediate syndrome which can occur between 24-96 hours (1-4 days) after organophosphate poisoning
Nervous system examination Organophosphorus induced delayed polyneuropathy is unrelated to acetylcholinesterase inhibition and occurs because of inhibition of other enzymes, in particular neurotoxic target esterase. It is characterised by demyelination of long nerves, when neurological dysfunction occurs 1-3 weeks after an acute exposure, particularly motor dysfunction but also sensory dysfunction, which may be chronic or recurrent
In addition, specific associations have been reported between chronic exposure of agricultural pesticides and autism spectrum disorders (ASD)
Nervous system examination
Organophosphorus induced delayed polyneuropathy is unrelated to acetylcholinesterase inhibition and occurs because of inhibition of other enzymes, in particular neurotoxic target esterase. It is characterised by demyelination of long nerves, when neurological dysfunction occurs 1-3 weeks after an acute exposure, particularly motor dysfunction but also sensory dysfunction, which may be chronic or recurrent
In addition, specific associations have been reported between chronic exposure of agricultural pesticides and autism spectrum disorders (ASD)
Random blood sugar levels Blood sugar changes may occur due to organophosphate poisoning.
When there is an accumulation of acetylcholine (ACh) at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system which can cause hypoglycemia
Random blood sugar levels
Blood sugar changes may occur due to organophosphate poisoning.
When there is an accumulation of acetylcholine (ACh) at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system which can cause hypoglycemia
Arterial blood gas analysis Organophosphate poisoning can cause acidosis Arterial blood gas analysis
Organophosphate poisoning can cause acidosis

Management - Supportive

Fact Explanation
Emergency management Quickly establish a patent airway, ensure adequate respiration and pulse. In cases of respiratory compromise secure airway and respiration via endotracheal intubation.Treat patients who have bronchospasm with an aerosolized bronchodilator. Intra venous fluid may be required to maintain the circulation Emergency management
Quickly establish a patent airway, ensure adequate respiration and pulse. In cases of respiratory compromise secure airway and respiration via endotracheal intubation.Treat patients who have bronchospasm with an aerosolized bronchodilator. Intra venous fluid may be required to maintain the circulation
Parent education Parents should teach young children about the dangers of poisons, beginning at an early age. Advise the parents about the proper storage and labeling of harmful pesticides Parent education
Parents should teach young children about the dangers of poisons, beginning at an early age. Advise the parents about the proper storage and labeling of harmful pesticides

Management - Specific

Fact Explanation
Decontamination - skin Important as the chemicals can be absorbed through skin.Clothes should be removed.Skin decontamination is accomplished with a shower using soap, large amounts of water Decontamination - skin
Important as the chemicals can be absorbed through skin.Clothes should be removed.Skin decontamination is accomplished with a shower using soap, large amounts of water
Decontamination- gastrointestinal Gastric lavage should be considered if patient presents within 60 minutes of ingestion.
Attempt aspiration first, followed by 100 to 200 mL normal saline, then aspiration
Activated charcoal is to be considered if patient presents within 60 minutes of ingestion
Decontamination- gastrointestinal
Gastric lavage should be considered if patient presents within 60 minutes of ingestion.
Attempt aspiration first, followed by 100 to 200 mL normal saline, then aspiration
Activated charcoal is to be considered if patient presents within 60 minutes of ingestion
Organophosphate poisoning Atropine (preservative-free, if possible), 2 to 5 mg IV every 15 minutes ( children >12 years) until pulmonary symptoms controlled; children < 12 years, 0.05 to 0.1 mg/kg every 15 minutes; doses repeated as needed for symptom control (up to 24 hours, taper dose)
Pralidoxime- IV 20 to 50 mg/kg (<12 years) over 30 minutes; repeated in 1 to 2 hours and at 10- to 12-hour intervals as needed for symptom control; alternatively: continuous IV infusion 10 to 20 mg/kg/hr (up to 500 mg/hr) after initial bolus and continued for 24 hours
Benzodiazepine for seizures (diazepam [Valium]), 5 to 10 mg slow IV push, repeated every 5 to 10 minutes to control or maximum 30 mg in adults; 0.2 to 0.5 mg/kg IV every 5 minutes to maximum of 10 mg in children >5 years, 5 mg in children <5 years; lorazepam may also be used
Organophosphate poisoning
Atropine (preservative-free, if possible), 2 to 5 mg IV every 15 minutes ( children >12 years) until pulmonary symptoms controlled; children < 12 years, 0.05 to 0.1 mg/kg every 15 minutes; doses repeated as needed for symptom control (up to 24 hours, taper dose)
Pralidoxime- IV 20 to 50 mg/kg (<12 years) over 30 minutes; repeated in 1 to 2 hours and at 10- to 12-hour intervals as needed for symptom control; alternatively: continuous IV infusion 10 to 20 mg/kg/hr (up to 500 mg/hr) after initial bolus and continued for 24 hours
Benzodiazepine for seizures (diazepam [Valium]), 5 to 10 mg slow IV push, repeated every 5 to 10 minutes to control or maximum 30 mg in adults; 0.2 to 0.5 mg/kg IV every 5 minutes to maximum of 10 mg in children >5 years, 5 mg in children <5 years; lorazepam may also be used
Carbamate poisoning Atropine IV (preferably or IM) children >12 years, 2.0 to 4.0 mg every 15 minutes until secretions controlled; children <12 years, 0.05 to 0.10 mg/kg every 15 minutes until secretions controlled; continue 2 to 12 hours; continued signs of poisoning indicate need for more atropine Carbamate poisoning
Atropine IV (preferably or IM) children >12 years, 2.0 to 4.0 mg every 15 minutes until secretions controlled; children <12 years, 0.05 to 0.10 mg/kg every 15 minutes until secretions controlled; continue 2 to 12 hours; continued signs of poisoning indicate need for more atropine

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