Defonition to management of organophosphate poisoning

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Organophosphate Poisoning
 COLLEGE OF MEDICAL SCIENCES
 DEPARTMENT OF PAEDIATRICS
 GOMBE STATE UNIVERSITY
 PRESENTERS; UG20/MDMD/1010
UG20/MDMD/1008
 MODERATOR; DR Fatima Musa
 Date; 21th August,2025

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OUTLINE
 INTRODUCTION
 EPIDEMIOLOGY
 BRIEF PHYSIOLOGY REVISION
 PATHOPHYSIOLOGY
 CLINICAL FEATURES
 INVESTIGATIONS
 MANAGEMENT
 CONCLUSION

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INTRODUCTION
What are organophosphates?
Organophosphates are chemical agents that comprise
the ester, amide or thiol derivatives of phosphoric acid
 They are commonly used as pesticides, herbicides, in
industries, agriculture, field sprays, household chemicals
and nerve agents in chemical warfare
 Most organophosphate poisoning occur as a result of
accidental exposure around the home or farm.

4.  Organophosphate poisoning continues to be a frequent
reason for admission to hospitals and intensive care unit in
developing countries (e.g Nigeria ) the traditional
approach to clinical features in acute OP poisoning has
centered on receptor specific effects on muscarinic,
nicotinic and CNS receptors.

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EPIDEMIOLOGY
 World wide pesticides poisonings cause an estimated
20,000 deaths and more than one million serious
poisonings annually.
 Children are at increased risk particularly in sub-Saharan
Africa due to the widespread use of pesticides
 A growing concern in chemical warfare and terrorism (e.g
nerve gas attack).

6. Physiology brief revision

7. Physiology brief revision

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PATHOPHYSIOLOGY
 Most organophosphates are highly lipid soluble
compounds and are well absorbed from intact skin, oral
mucus membranes, conjunctiva and the gastrointestinal
and respiratory tracts
 The highest concentration is found in the liver and kidneys
 Due to high lipid solubility they easily cross the blood brain
barrier

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PATHOPHYSIOLOGY
 Organophosphates produce toxicity by binding to and
inhibiting to acetylcholinesterase enzyme preventing
degradation of acetylcholine resulting in its
accumulation at nerve synapses
 If left untreated it irreversibly binds to the enzyme
leading to its permanent inactivation
 This process is called aging

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PATHOPHYISOLOGY
 This process occurs over a variable period of time
depending on the characteristics of specific
organophosphate
 Accumulation of Acetylcholine leads to increase
muscarinic effects at the postganglionic
parasympathetic synapses,
 This causes smooth muscle contractions in the GI
tract, bladder, and secretory glands.

11. Pathophysiology

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CLINICAL PRESENTATION
 Patients usually present with history of exposure by means of
ingestion, inhalation or dermal exposure
 Symptoms are due to accumulation of Ach at the peripheral
nicotinic and muscarinic synapses and in the CNS.

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CLINICAL PRESENTATION
Symptoms due to cholinergic excess at the muscarinic
receptors include
 Diarrhea/defecation
 Urination
 Miosis
 Bronchospasm
 Bradycardia
 Emesis
 Lacrimation
 Salivation

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CLINICAL PRESENTATION
Nicotinic signs and symptoms include;
 Muscle weakness
 Fasciculation
 Tremors
 Hypoventilation(diaphragm weakness)
 Hypertension
 Tachycardia and dysrhythmias
 Severe manifestations include coma, seizures and shock

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INVESTIGATIONS
 RBC cholinesterase and pseudocholinesterase activity
 Full blood count
 Electrolytes, urea and creatinine
 CXR
 ECG

16. CXR Investigation findings
 Chest X-ray reveals pulmonary edema, aspiration
pneumonitis, infiltrates or consolidation in the lungs

17. ECG Investigation findings

18. E/U/Cr Investigation findings
 Creatinine elevated
 Blood urea nitrogen elevated
 Hypokalemia
 Hyponatremia or hypernatremia
 Low bicarbonate levels

19. Full blood count findings
 FBC reveals unspecific findings and the cholinesterase
and pseudo cholinesterase activity is markedly reduced

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DIAGNOSIS
 Diagnosis of organophosphate poisoining is based
primarily on history and physical examination
 Garlic-like smell is an added clinical sign especially if
patient ingested sulphur containing OP compound

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TREATMENT
Principles of treatment include;
1.Decontamination and Rescucitation
2. Blockade of muscarinic activity
3. Reversal of cholinesterase inhibition
4. Management of complications

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TREATMENT
 Decontamination includes washing all exposed body parts with
soap and water and immediately removing all exposed
clothings
 Gastric lavage should be considered if patient presents within
2hrs of ingestion
 Decontamination with activated charcoal is of unlikely benefit
 Resuscitation includes assessment of the airway, breathing and
circulation
 Intubation and fluid and electrolyte replacement if necessary

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TREATMENT
Blockade of muscarinic activity;
 This is done by giving atropine as antidote, it is given 0.05-0.1
mg/kg intravenously
 it antagonizes the muscarinic ach receptor
 Atropine dosing is primarily targeted to drying the respiratory
secretions

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TREATMENT
Reversal of cholinesterase inhibition;
 This is achieved by giving pralidoxime as an antidote, it is
given 25-50mg/kg over 5-10mins (max: 200mg/min), can
be repeated after 1-2hr, then 10-12 hourly as needed
 It breaks the bond between the organophosphate and
the ach enzyme
 It is given before the bond ages and becomes permanent

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CONCLUSION
 Organophosphate poisoning is a common accidental
poisoning prevalent in children less than six years, it is more
prevalent in developing countries, early diagnosis and
prompt treatment is key in good prognostic outcomes.

26. 26 REFERENCES
 Nelson Textbook of paediatrics 21st
edition
 Management of toxic exposure in children. Emergency
med clinic north am 2003
 Organophosphate insecticide intoxication in children, int j
emerg med 2011
 Senarathna L, Jayamanna SF, Kelly PJ, Buckley NA, Dibley
MJ,
 Dawson AH. Changing epidemiologic patterns of
deliberate self
 poisoning in a rural district of Sri Lanka. BMC Public Health
 2012;12:593.
 2. Balme KH, Roberts JC, Glasstone M, Curling L, Rother HA,
London L,

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