ORGANOPHOSPHORUS COMPOUNDS & CLINICAL

FEATURESPresenter :Dr.Milan Bhusal

HISTORY First synthesized in early 1800 by Lassaigne

Lange and Schrader investigated the use as insecticides

German Military prevented the use; developed arsenal for chemical warfare

In 1941, re-introduced worldwide for pesticide use

Used in various terrorist attacks and regional wars

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OP COMPOUNDS

Dichlorvos Fenthion Malathion Ethion

Diazinon Parathion Chlorpyrifos

DIMETHYL COMPOUNDS DIETHYL COMPOUNDS

NERVE AGENTS G agents- Sarin, Tabun, Soman V agents- VX, VE

INSECTICIDES

Inhibit esterase enzymes

Acetylcholinesterase in synapses and on red cell membranes & Butyrylcholinesterase in plasma

Accumulation of ACh and overstimulation of ACh receptors in synapses of ANS, CNS and NMJ

Recovery Aging

MECHANISM OF ACTION

Common OP compounds available in Nepal

National poison information centre:

9851038490

Clinical features:

IV/IM within 30 min.

Oral or respiratory exposures - signs or symptoms within three hours.

Symptoms of toxicity from dermal absorption - delayed 12 hours.

INHALATION Cough Difficulty in breathing Bronchitis Pneumonia

EYE CONTACT Irritation Pain Lacrimation Miosis Blurring vision Photophobia

SIGNS AND SYMPTOMS

MUSCARINIC EFFECTS

NICOTINIC EFFECTS

CNS EFFECTS

NEUROPSYCHIATRIC EFFECTS

MUSCARINIC:

Cardiovascular : Bradycardia, hypotension

Respiratory : Rhinorrhea, bronchorrhea, bronchospasm, cough, severe respiratory distress

Gastrointestinal : Hypersalivation, nausea and vomiting, abdominal pain, diarrhea, fecal incontinence

Genitourinary: Incontinence

Ocular: Blurred vision, miosis

Glands : Increased lacrimation, diaphoresis

CLINICAL PRESENTATIONMUSCARINIC: SLUDGE

S-SalivationL-LacrimationU-UrinationD-DiarrhoeaG-GI upsetE-Emesis

NICOTINIC: MATCHM-Muscle weakness and fasciculationA-Adrenal medulla activity ↑T-TachycardiaC-Cramping of skeletal muscleH-Hypertension

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CNS EFFECTS @C.E.A.S.T.A.R. Anxiety

Emotional liability

Restlessness

Confusion

Ataxia

Tremors

Seizures and coma

Neuropsychiatric effects

Chronic

Headache, blurred vision, muscle weakness, depression, memory and concentration problem

The mechanism is not proven

NEUROLOGICAL MANIFESTATIONS:

Type I paralysis or Acute paralysis.

Type II paralysis or Intermediate syndrome.

Type III paralysis or Organophosphate- induced delayed polyneuropathy(OPIDP)

Type 1 paralysis or Acute paralysis

Muscles fasculations ,

Muscles cramps.

Twitching and weakness

Respiratory muscles weakness and paralysis.

CNS depression.

Respiratory arrest.

TYPE II (INTERMEDIATE SYNDROME):

Develops after 24-96 hours ; persists 4-18 days

Respiratory distress, weakness of proximal muscles, neck and trunk, with relative sparing of distal muscles

Doesn’t respond to oximes or atropine, needs assisted ventilation

Recovery in 5-18 days

IMS AND OPIDPIMS Time of onset 1-4 days Proximal limb muscle

weakness Neck muscle + Respiratory muscles + Recovery time 4-18 days Agents: Fenthion, Dimethoate,

Monocrotophos

OPIDP Time of onset 2-3 weeks Distal limb muscle weakness Neck muscle - Respiratory muscles - Recovery incomplete Agents: Methamedophos,

Trichlorfon, Leptophos

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 TYPE III PARALYSIS: Delayed polyneuropathy

Occurs 2-3 weeks after exposure to large doses of certain organophosphates, last up to 12 months

Damage to the afferent fibres and associated inhibition of neuropathy target esterase

Distal muscle weakness/paralysis/paresthesia with sparing of the neck muscles, cranial nerves and proximal muscles Recovery incomplete