Types of organophosphate insecticides
- Diazinon-phosphorothioic acid
Route of absorption/poisoning;
- ingestion(accidental or suicidal)
- injection (intramascular or intravenous)
Organophosphate are absorbed through the skin lungs & GI tract and distributed widely in tissues and are slowly eliminated in hepatic metabolism.The principal effect is inhibition of cholinesterase enzymes, particularly acetylcholinesterase (AChE). This leads to accumulation of acetylcholine at;
- Muscarinic receptors- in cholinergic receptor cell.
- Nicotinic receptors – in skeletal neuromuscular junction and autonomic ganglia.
- centraL nervous system(CNS).
1.There is always history of;
- Dermal absorption
NB: Features of intoxication are usually delayed i.e. because the poison requires biotransformation to become active.
3.Muscarinic effects of Poisoning are characterized by;
- Abdominal colic, cramps
- Dyspnoea due to bronchoconstiction
- Chest tightness
- Urinary and fecal incontinence,
- Muscle fasciculation
- Flaccid paralysis
- Limbs muscles weakness/tremors
- Respiratory muscles weakness
- ocular muscles weakness
Respiratory failure is worsened/exacerbated by development of rhinorrhoea and pulmonary Oedema
Central Nervous system
This occurs in severe poisoning and features include;
- loss of memory
- convulsion and
8.Organophosphate induced neuropathy
- Starts two weeks or more after exposure
- Occurs due to degeneration of mylenated motor & sensory fibres
1.Exposure is confirmed by measurement of plasma(butyrycholinesterase) or red blood cell cholisterase activity. These correlate poorly with the severity of clinical features, although values are usually less than 10% in severe poisoning,20%-50% in moderate poisoning and > 50% in subclinical poisoning.
2 Others investigations ;
- Chest x-ray – to evaluate pulmonary oedema
- Urea, electrolytes and creatinine
- ECG to monitor cardiac arrhythmias
Management of organophosphate poisoning.
Patients who are seriously poisoned must be identified early so that appropriate management is not delayed. Triage involves:
- Immediate measurement of vital signs
- Identifying the poison(s) involved and obtaining adequate information about them
- Identifying patients at risk of further attempts at self-harm and removing any remaining hazards from them.
Those with external contamination with chemical or environmental toxins should undergo appropriate decontamination. Critically ill patients must be resuscitated.
1.For mild cases
No specific treatment;
- Clearing the Airway,
- Adequate ventilation-consider oxygenation
- Remove soiled clothes
- Wash contaminated skin to prevent further absorption
2.Patient with systemic features
Early use of sufficient doses of atropine is potentially life-saving in patients with severe toxicity.
Patients with systemic features
i) IV atropine 0.6 – 2mgs every 10- 15 minutes till signs of atropinization are seen (dry skin, dilated pupils and reduced bronchial secretions)
mode of action of atropine;
- Reduces – Bronchorrhoea & Rhinorrhoea & wheezing
- It is a beta adrenoceptor blocking drug.
ii) Add an OXIME e.g. Pralidoxime
- Dose – Slow IV injection 30mgs/kg every 4-6 hours i.e. 1-2gms iv or infusion 8-10mg/kg/h i.e. 200-400mgs/h
mode of action
- Reactivates phophorylated acetyl cholinesterase.
- Prevents permanent binding of the organophosphate to cholinesterase.
iii) Gastric lavage within an hour post poisoning, followed by activated charcoal administered via nasogastric tube.
iv) Wash the patient – to prevent dermal absorption
v) Wash soiled clothes
vi) Monitor patient 2 hourly in left lateral position
Vii) Consider ICU care if in coma or unconscious ;
- Benzodiazepines may be used to reduce agitation and fasciculations, treat convulsions and sedate patients during mechanical ventilation.
viii) intravenous fluids ; to flush out toxin from body.
x) Counselling; once patient is stable counselling should be initiated.
i.Respiratory failure – this is due to respiratory muscle paralysis, bronchial constriction and copious respiratory secretions.
ii.Hyperglycaemia, complete heart block and arrhythmias occurs in severely poisoned patients.
iii.Intermediate syndrome. Consists of cranial nerve and brain stem lesions, and proximal neuropathy.
- Commence 1-4 days after acute poisoning lasting for approximates 3 weeks
- Unresponsive to atropine and Oximes
iv.Organophosphate induced delayed Neuropathy
- Starts 2 weeks or more after exposure
- It is as a result of degeneration of large myelinated motor and sensory fibres.
Something to Note
- Initial flaccidity and muscle weakness in the arms and legs give rise to a clumsy shuffling gait and followed later by spasticity, Hypertonicity, Hyperreflexia, and clonus.
- Patients with damage to lower exteremities such as foot drop is permanent.
- Haemoperfusion and haemodialysis are of no benefit in patients with organophosphate poisoning.
- OXIMES. Are cholinesterase reactivators. Examples include, Pralidoxime (P2S) and Obidoxime (toxogonin). This drugs are helpful if given before the organophosphorus-cholinestrase enzymes complex ‘ages.