| Fact | Explanation |
|---|---|
| Anxiety[1], seizures [3],headache, dizziness [1] | 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 [2] |
| Muscle twitching, muscle weakness [1] | Nicotinic effects due to excess acetylcholine [2] |
| sweating, salivation, diarrhea, tearing [1] | Muscarinic effects due to excess acetylcholine [2] |
| Breathing difficulty [4] | 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 [2] |
| Unconscious [1] | 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 ) [2] |
| Fact | Explanation |
|---|---|
| Hypertension [1] | When there is an accumulation of acetylcholine (ACh) at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system [2] |
| Bradycardia [1] | Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh leads to depression of circulation [2] |
| Convulsions [1] | 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 [2] |
| Miosis [1] | Effects of organophosphate poisoning on muscarinic receptors (excess acetylcholine) [2] |
| Dyspnea , ronchi [3] | 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 [2] |
| Fact | Explanation |
|---|---|
| Cyanide poisoning [1] | Very rapid onset of symptoms in seconds or minutes with gasping, air hunger and acidosis. There are confusion, convulsions, collapse and coma. There is decreased respiratory rate, respiratory arrest or sudden death. Cyanosis is unusual but there may be cherry pink skin (only seen postmortem in carbon monoxide poisoning). Pupils are dilated or normal with no fasciculation and secretions are normal [1] |
| Fact | Explanation |
|---|---|
| Plasma choline esterase levels / levels of OP metabolites [1] | 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[1] |
| Fact | Explanation |
|---|---|
| Random blood sugar levels [1] | 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 [1] |
| Fact | Explanation |
|---|---|
| Tendon reflexes [1] | 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 [1] |
| Nervous system examination [1] | 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 [1] In addition, specific associations have been reported between chronic exposure of agricultural pesticides and autism spectrum disorders (ASD) [2] |
| Fact | Explanation |
|---|---|
| Arterial blood gas analysis [1] | Organophosphate poisoning can cause acidosis [1] |
| Fact | Explanation |
|---|---|
| Emergency management [1] | 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 [1] |
| Parent education [1] | 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 [1] |
| Fact | Explanation |
|---|---|
| Decontamination - skin [1] | 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 [1] |
| Decontamination- gastrointestinal [1] | 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 [1] |
| Organophosphate poisoning [1] | 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 [1] |
| Carbamate poisoning [1] | 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 [1] |