What should know about organophosphate poisoning.

Organophosphate poisoning is poisoning due to organophosphates (OPs).Organophosphate poisoning occurs most commonly as a suicide attempt in farming areas and less commonly by accident. This mostly occurs in developing world. Organophosphates are chemicals in insecticide used extensively in agriculture. When people, such as agricultural workers, are exposed to large quantities of organophosphates, these chemicals can be harmful.

Types of organophosphate insecticides

  • Diazinon-phosphorothioic acid
  • chlorpyrifos
  • malathion
  • parathion
  • fenthion
  • sarin
Danger poison
Danger poison sign post pic

Route of absorption/poisoning;

  • cutaneously
  • ingestion(accidental or suicidal)
  • inhalation
  • injection (intramascular or intravenous)

pathophysiology

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;

  1. Muscarinic receptors- in cholinergic receptor cell.
  2. Nicotinic receptors – in skeletal neuromuscular junction and autonomic ganglia.
  3. centraL nervous system(CNS).

Clinical features

1.There is  always history of;

  • Ingestion
  • Inhalation
  • 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;

  • Anxiety
  • Restless
  • Tiredness
  • Vomiting
  • Abdominal colic, cramps
  • Diarrhea
  • Tenesmus
  • Sweating
  • Rhinorrhoea
  • Bronchorrhoea
  • Dyspnoea due to bronchoconstiction
  • Chest tightness
  • Nausea,
  • Urinary and fecal incontinence,
  • Lacrimation
  • wheeze
  • Miosis
Miosis due organophospates poisoning
excessive pupils constriction pic

4.Nicotinic effects

  • Muscle fasciculation
  • Flaccid paralysis
  • Limbs muscles weakness/tremors
  • Respiratory muscles weakness
  • ocular muscles weakness

5.Respiratory system

Respiratory failure is worsened/exacerbated by development of rhinorrhoea and pulmonary Oedema

Central Nervous system

This  occurs in severe poisoning and features include;

  • headache
  • anxiety
  • loss of memory
  • convulsion and
  • coma.

8.Organophosphate induced neuropathy

  • Starts two weeks or more after exposure
  • Occurs due to degeneration of  mylenated motor & sensory fibres

Investigations include;

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.

General approach.

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.

ix) Antacids.

viii) intravenous fluids ; to flush out toxin from body.

x) Counselling; once patient is stable counselling should be initiated.

Complications Includes

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.

 

 

 

 

 

 

 

About Docbobhe 26 Articles
Am Robert Mathenge, a healthcare provider in Nakuru county. i love this profession as it gives me chance to serve my call, interacting with people from various social backgrounds makes me feel good.

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