Organophosphorus (OP) poisoning is a major cause of morbidity and mortality in Nepal. OP compounds inhibit acetylcholinesterase, leading to accumulation of acetylcholine and overstimulation of nicotinic and muscarinic receptors. Common presentations include excessive sweating, salivation, vomiting, diarrhea, bronchospasm, bradycardia, hypotension. Treatment involves atropine to block muscarinic effects, pralidoxime to reactivate acetylcholinesterase, benzodiazepines for seizures, and supportive care. Prognosis depends on severity of cholinergic crisis, and intermediate syndrome occurring 1-4 days later can cause respiratory failure if not properly managed.
Please find the power point on Organophosphate poisoning and its management. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Please find the power point on Organophosphate poisoning and its management. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Please find the power point on Paracetamol poisoning. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Organophosphate poisoning is poisoning due to organophosphates (OPs). Organophosphates are used as insecticides, medications, and nerve agents.
Symptoms include increased saliva and tear production, diarrhea, vomiting, small pupils, sweating, muscle tremors, and confusion.
Other names: Organophosphate toxicity
Causes: organophosphates
Please find the power point on Paracetamol poisoning. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Organophosphate poisoning is poisoning due to organophosphates (OPs). Organophosphates are used as insecticides, medications, and nerve agents.
Symptoms include increased saliva and tear production, diarrhea, vomiting, small pupils, sweating, muscle tremors, and confusion.
Other names: Organophosphate toxicity
Causes: organophosphates
Clinical symptoms and management of poisoningschiragmarwah1
This presentation contains relevant and genuine information regarding clinical symptoms and management of different types of poisonings such as Barbiturate poisoning, Morphine poisoning, Arsenic Poisoning, Organophosphate poisoning, and Lead Poisoning. Hopefully the contents in presentation will help the pharma students to understand the concept of poisoning in a better and appropriate way.
Regards:
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Organophosphate poisoning national guidelinecharithwg
publication by Dr-C.Here the given information are based on recommendations by sri lankan medical specialists who have dealt with the issue for a long time. it is quite obvious using agro chemical to deliberate self harm is a tendency in developing countries. it is common in agricultural ares.all the information are correct according to my knowledge. all the materials used to publish the slideshow are international publications. you have the full right to download and read. my personal request is to submit your ideas to me. and suggest different topics. i like to see your responses. i hope you would manage patients like these some day though it is so sad to see such incidents. be confident. do good. do not harm. be kind. keep us in your memories.
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In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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2. • Poisoning has been a common cause of medical admissions and
deaths in Nepalese hospitals.
• 31% of all suicidal deaths are due to poisoning.
• OP compounds were the most common form of poisoning - 52% of
total cases.
• occupy the greatest burden of poisoning related morbidity and
mortality in Nepal
3. Compounds
• first used as an agricultural insecticide and later as potential chemical
warfare agents.
• are normally esters, thiol esters, or acid anhydride derivatives of
phosphorus containing acids.
• >100 OP pesticides used worldwide, the majority are dimethyl
phosphoryl or diethyl phosphoryl compounds.
• Nerve gas compounds like tabun, sarin, and soman are highly potent
synthetic toxic agents of this group.
6. Mechanism of action
• OP compounds phosphonylate
the active site of
acetylcholinesterase (AChE),
inactivating the enzyme
• leading to the accumulation of
acetylcholine (ACh) in
cholinergic synapses
7. • Spontaneous hydrolysis of the OP-enzyme
complex allows reactivation of the enzyme.
• AChE-dimethyl OP complex spontaneously
reactivate in less than one day
• AChE-diethyl OP complex may take several
days and reinhibition of the newly activated
enzyme can occur significantly
• spontaneous reactivation can be hastened
by adding nucleophilic reagents like oximes,
liberating more active enzymes.
8. • loss of a chemical group from the OP-
enzyme complex prevents further
enzyme reactivation, a process termed
‘ageing’.
• After ageing has taken place, new
enzyme needs to be synthesised before
function can be restored.
9. • rate of ageing is an important determinant of toxicity
• dimethyl compounds (3.7 hours)
• diethyl compounds (31 hours)
• rapid after exposure to nerve agents (soman in particular) -ageing
within minutes
10. Signs and symptoms of OPC poisoning
Four clinical syndromes have been described:
1. Acute cholinergic syndrome (most common)
2. Sub acute proximal weakness (Intermediate syndrome)
3. Organophosphate induced delayed neuropathy (OPIDN)
4. Chronic organophosphate induced neuropsychiatric disorder (COPIND)
14. Intermediate syndrome
• usually occurs 24 to 96 hours after the ingestion of an OP compound
• after an initial cholinergic crisis but before the expected onset of
delayed polyneuropathy.
• Approximately 10-40% of patients treated for acute poisoning
develop this illness.
• characterized by prominent weakness of neck flexors, muscles of
respiration and proximal limb muscles.
• Mostly seen with fenthion, dimethoate and monocrotophos,
15. • muscle weakness may last up to 5-14 days
• condition regresses slowly if respiratory support is available.
• exact pathogenesis is unclear, the proposed mechanisms include
persistent inhibition of AChE leading to functional paralysis of
neuromuscular transmission, muscle necrosis, and oxidative free
radical damage to the receptors.
16. Delayed Polyneuropathy
• is an uncommon consequence of severe intoxication or intermittent and
chronic contact with OP pesticides as in occupational exposure.
• is due to inhibition of neuropathy target esterase (NTE) enzyme in nervous
tissues by certain OP compounds.
• often unrecognized in humans.
• distal symmetric sensory-motor polyneuropathy (distal weakness,
parasthesia, ataxia, diminished or absent reflexes).
• symptoms usually begin 2-5 weeks after exposure, and may last for years.
• OP pesticides can also cause chronic neurotoxicity and behavioural
impairment in some patients
17. Diagnosis
History and clinical features
• History of ingestion, availability of bottles
• typical clinical symptoms and signs help to diagnose the OP
poisoning.
• characteristic petroleum or garlic – like odour, which may be helpful
in establishing the diagnosis
18. Atropine challenge
• If doubt exists, a trial of 1 mg atropine in adults (or 0.01 to 0.02
mg/kg in children) may be employed.
• absence of signs or symptoms of anticholinergic effects following
atropine challenge strongly supports the diagnosis of poisoning with
an acetylcholinesterase inhibitor
• If pulse rate goes up by 25 per minute or skin flushing develops
patient has mild or no toxicity
19. RBC acetylcholinesterase
• Direct measurement of RBC acetylcholinesterase (RBC AChE) activity
provides the measure of the degree of toxicity
• the test is not usually available.
plasma (or pseudo) cholinesterase activity
• is more easily performed
• does not correlate well with severity of poisoning
• should not be used to guide therapy.
AChE and PChE activity can fall to about 80% of normal before any symptoms
occur and drop to 40% of normal before the symptoms become severe.
20. Chemical analysis of vomitus or gastric aspiration
• may identify the poison.
• Chemical analysis may also be particularly important in case of self-
poisoning using multiple compounds.
• Thus, after gastric lavage or vomiting, the aspirate or vomitus should
be preserved.
21. Grading of severity of poisoning
• Clinical Grading (Peradeniya organophosphorous score)
• Biochemical Grading
23. Biochemical Grading:
Red cell cholinesterase activity (% normal) Grade
• 20-50% Mild
• 10-20% Moderate
• <10% Severe
24. Treatment
General measures
• Rapid initial assessment of airways, breathing, and
circulation is essential.
• Comatose or vomiting patients should be kept in
lateral, preferably head down position with neck
extension to reduce the risk of aspiration.
• airway should be secured with proper positioning,
placement of Guedel’s airway or with endotracheal
intubation Frequent suctioning
• Oxygen
• clothes should be removed and the skin vigorously
washed with soap and water.
25. Gastric lavage
• may help to reduce the absorption of the ingested poison and should
be considered in patients presenting within 1-2 hours of ingestion of
poison.
• risks of gastric lavage include
• aspiration,
• hypoxia, and
• laryngeal spasm,
26. Treatment of Acute Toxicity
Atropine
• 2 – 5 mg IV bolus (0.05 mg/kg IV in children). (each ampoule
containing 0.6 mg)
• Check three things after five minutes: pulse, blood pressure and chest
crackles.
• Aim for heart rate >80 beats per minute, SBP > 80 mm Hg, and a
clear chest (atropine won't dry focal areas of aspiration).
• Double the atropine dose every five minutes if you have not achieved
these objectives.
27. • Review patient every 5 min.
• Once these parameters start improving, repeat last same or smaller
dose of atropine.
• If improvement in these parameters is persistent and satisfactory
after 5 min, now you can plan for atropine infusion.
28. Target end-points for Atropine therapy
• Heart rate >80/ min
• Dilated pupils
• Dry axillae
• Systolic blood pressure >80 mm Hg
• Clear chest with absence of wheeze
29. • When the patient achieves most of (at least 4 out of 5) the target
end-points for atropine therapy i.e., ‘fully atropinized’, an intravenous
infusion is set up to maintain the therapeutic effects of atropine.
• use 20% of initial atropinizing dose per hour for first 48 hours and
gradually taper over 5 -10 days, continuously monitoring the
adequacy of therapy.
30. • Atropine toxicity can result in
• agitation,
• confusion,
• hyperthermia,
• severe tachycardia
• can precipitate ischaemic events in patients with underlying coronary
artery disease.
31. Management of Atropine toxicity
• Stop the atropine infusion
• Check again after 30 min to see whether the features of toxicity have
settled
• If not, continue to review every 30 min or so
• When they do settle, restart at 70–80% of the previous rate
• The patient should then be seen frequently to ensure that the new
infusion rate has reduced the signs of atropine toxicity without
permitting the reappearance of cholinergic signs
32. Pralidoxime
• recommended in patients with evidence of cholinergic toxicity in
patients with organophosphorous poisoning.
• PAM is not recommended for poisoning due to carbamate poisoning.
• The standard recommended dose of PAM is 2 g (25 – 50 mg/kg in
children) IV over 30 minutes, with continue infusion at 8 mg/kg/hour
in adults (10 – 20 mg/kg/hour in children)
• Alternate dose- 1 gm of bolus followed by 0.5 to 1 gm 6 to 8 hourly in
adult patient.
• can be continued as per the severity of poisoning.
33. Point to remember
• Pralidoxime should not be administered without concurrent atropine,
to prevent worsening symptoms due to transient oxime induced
acetylcholinesterase inhibition
• Even the bolus dose of PAM is administered slowly
• a fast infusion can cause vomiting, hypertension, cardiac arrhythmia
or a cardiac arrest.
34. Giving fluids/ IV channel
Two IV drips should be set up
One for fluid and drugs. Give 500–1000 ml (10–20 ml/kg) of
normal saline
Other for atropine
35. Benzodiazepine therapy
• Diazepam 0.1 – 0.2 mg/kg/ IV,
• repeated as necessary, if seizures occur.
• early use of diazepam may reduce morbidity and mortality
36. Cause of Death in OPC poisoning
1. Immediate death:
– Seizures.
– Complex ventricular arrhythmias.
2. Death within 24 hours:
- Acute cholinergic crisis in untreated severe case
-Respiratory failure.
3. Death within 10 days of poisoning:
- intermediate syndrome.
Contd.
37. Cause of Death in OPC poisoning
3. Death within 10 days of poisoning:
- intermediate syndrome.
4. Late death:
- Secondary to ventricular arrhythmias, including Torsades de
Pointes, which may occur up to 15 days after acute
intoxication.
Methyl-parathion, Dichlorovos, Dimethoate,
Chlorpyrifos and Malathion are the common OPs related
with human poisoning.
‘Metacid’ (Methyl parathion) is the most frequently ingested and
probably the most toxic organophosphate used for
poisoning in Nepal.
Dichlorovos, or ‘Nuvan’ as it is
commonly known, is moderately volatile solution; its
use has been on rise for self harm in recent years.
Dimethoate has a lethal dose of 10-12 gm and there
are concerns that it causes specific cardiac toxicities in
addition to cholinergic syndrome.
Malathion is relatively less-toxic ,used for the treatment of pediculosis
and scabies in humans; and has a lethal dose is 1 gm/kg
in mammals
The induction of vomiting with soap water, ipecacuanha or other agents
may cause more harm than benefit as many OPs are
dissolved in petroleum distillates and can cause severe
pneumonitis and acute respiratory distress syndrome
when aspirated.
Use of home remedies like ingestion
of milk may dilute the poison but risks increased
gastric emptying; and ‘pushing’ the poison into small
bowel from where it is readily absorbed with early
development of toxicity.
On the contrary small amount
of lipid-rich home remedy (e.g. raw eggs) may slow
gastric emptying and delay the onset of poisoning and
respiratory failure.