This document summarizes the clinical manifestations of organophosphorus and organochlorine poisoning. It describes how organophosphates work by inhibiting acetylcholinesterase, leading to increased acetylcholine levels and overstimulation of muscarinic and nicotinic receptors. Signs and symptoms are divided into muscarinic effects (SLUDGE), nicotinic effects, and CNS effects. Organochlorines are strongly lipid soluble and sequester in tissues, causing prolonged systemic effects. The document also outlines routes of absorption, presentations of acute and chronic toxicity, and introduces the Peradeniya Organophosphorus Poisoning scale for assessing severity without laboratory tests.

1. January 26, 2014
YUGAL JYOTY NEPAL
MODERATOR: Dr. Rabin Sharma
ORGANOPHOSPHORUS
AND ORGANOCHLORINE
POISONING
CLINICAL MANIFESTATIONS

2. How do Organophosphates work?
 Inactivate
Acetylcholinesterase
Choline
 Increase

Acetic acid
Acetylcholine level
ACh is found in the central and peripheral nervous system, neuromuscular
junctions, and red blood cells (RBCs)

3. Increased
Ach levels result in overstimulation of
muscarinic and nicotinic receptors

4. Overview
of
muscarinic
receptors

5. Overview
of
muscarinic
receptors
contd…

6. Overview
of
nicotinic
receptors

7. Routes of absorption
Organophosphates
absorbed
ingested
 inhaled
injected

can be
cutaneously

8. Although most patients rapidly become symptomatic,
the Onset and Severity of symptoms depend on
specific
compound
amount
route
rate
of exposure and
of metabolic degradation

9.  Signs
and symptoms of organophosphate poisoning
can be divided into 3 broad categories
1. muscarinic
2. nicotinic
3. CNS
effects
effects
effects

10. MUSCARINIC effects
SLUDGE
salivation, lacrimation, urination, diarrhea, GI upset, emesis
DUMBELS
diaphoresis and diarrhea
urination
miosis
bradycardia, bronchospasm, bronchorrhea
emesis
excess lacrimation
salivation

11. Muscarinic effects by organ systems include the following:
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

12. NICOTINIC effects
 muscle
fasciculations
 cramping
 Weakness
and
 diaphragmatic
failure
Autonomic nicotinic effects include
 Hypertension
 Tachycardia
 Mydriasis
 Pallor

13. CNS effects
 anxiety
 emotional
liability
 restlessness
 confusion
 ataxia
 tremors
 seizures
 coma

14. ORGANOCHLORINES
 Organic
chlorines are strongly lipid soluble and
sequester in body tissues with high lipid content, such
as the brain and liver
 Consequently,
blood levels tend to be much lower
than fatty tissue levels
 The
lipophilic tendency of organochlorines accounts
for prolonged systemic effects in overdose

15. Routes of absorption
 Ingestion
 Skin
absorption or inhalation
 Chronic
exposure

16. Ingestion produces the following manifestations:
Nausea
and vomiting
Confusion,
tremor, myoclonus, coma, and seizures
Respiratory
depression or failure
Unusual
odor

17. Skin absorption or inhalation produces the following
manifestations:
Ear,
nose, and throat irritation
Blurred
vision
Cough
Acute
lung injury (ALI)
Dermatitis

18. Long-term occupational exposure to organochlorine pesticides may
result in various nonspecific symptoms - headaches, nausea, fatigue,
muscle twitching, and visual disturbances
In addition, chronic exposure to these agents may be associated with
the development of blood dyscrasias, including aplastic anemia and
leukemia
Other manifestations of chronic exposure are as follows:
Anorexia
Hepatotoxicity
Renal
CNS
toxicity
disturbances

19. Presentation
 Onset
– abrupt
 CNS
excitation and depression are the primary effects
observed in acute organochlorine toxicity - The patient
may appear agitated, lethargic, intoxicated, or may even
be unconscious
 Initial
euphoria with auditory or visual hallucinations and
perceptual disturbances are common in the setting of
acute toxicity.

20. Peradeniya Organophosphorus Poisoning (POP) scale
 Laboratory
estimation of blood cholinesterase and OP levels are not
available in many developing countries
 POP
score can assess severity without laboratory investigation
 Also
patient co-ordination not required
The score is given when the patient first presents in the hospital
Nimal Senanayake, H.J. de Silva Kaealliedeand Laxman Karalleidde (Department of
Medicine, Faculty of Medicine, University of Perdeniya, Sri Lanka and Queen
Elizabeth Military Hospital, London, UK)

21. Parameter
Pupil size >2mm
0
Pupil size <=2mm
1
Pinpoint pupil
2
None
1.
Score
0
Miosis
2. Fasciculation
Present but not generalized or
continuous
1
Generalised and continuous
2
Respiratory rate <=20/min
0
Respiratory rate >20/min
1
Respirator rate >20/min with central cyanosis
2
3. Respiration
4. Bradycardia
Pulse rate >60/min
0
Pulse rate 41-60/min
1
Pulse rate <=40/min
2
Conscious and rational
0
Impaired, responds to verbal command
1
Impaired, no response to verbal command
2
If convulsions present, add
1
TOTAL
11
5.Level of consciousness

22.  POP
score 0-3 : Mild
 POP
score 4-7 : Moderate
 POP
score 8-11 : Severe
Based on results from the initial study, severe intoxications
(score of 8 to 11) have a higher mortality rate
Require greater need for ventilatory support, and higher
dose of atropine in the first 24 hours.

23. THANK YOU