INTRODUCTION
Clinical VignetteYou are posted as a CMO, casualty in the month
of June. A 30 year old housewife from a nearby village is brought
in the afternoon in an unconscious state. There is h/o domestic
violence. Patients clothes are wet and are soiled with urine and
feces.O/E pupils are constricted with BP= 80/60mmHg. You check
patients blood sugar level which is 480 mg%. You order an ABG which
is s/o metabolic acidosis. ECG is done and it shows bradycardia.
Routine blood workup reveals normal serum electrolytes with a
raised amylase level of 300.Diagnosis ??? ??
Organophosphorus Poisoning
Presentor : Dr Lohit Chauhan
INTRODUCTIONOP are a group of insecticides or nerve-agents which
act at acetyl-cholinesterase
Have been used as insecticides, petroleum additives and chemical
warfare agents
Carbamates are another group of insecticides which act at the
same site, with a slight different MOA
WHO CLASSIFICATION (simplified)HIGHLY TOXICMODERATELY TOXIC1.
Phosphamidon (Dimecron)1. Malathion2. Ethyl parathion2. Fenthion
(Baytex)3. Methyl parathion3. Temephos (abate)4. Chloro-thiophos 4.
Fenitrothin (tik-20)5. Carbo-phenothion5. Diazinon (spectacide)
* Shivakumar S, Ishaq RM. Management of Organophosphorus
compounds (OPC) Poisoning : Current Status 2008. taken from
drshivkumar.org
Epidemiology (WHO)Acute OP poisoning is one of the common and
serious medical emergencies
Asia : 3 million cases/ year of acute pesticide poisoning
3 lakh deaths per year (CFR =10-15 %)
99% cases are seen in developing world
Indian DataPoisoning is 4th MC cause of deaths annually
OP poisoning is the MC poisoning
Pattern of poisoning is region-dependant
OP poisoning is more common in south India
North India- aluminium phosphide > OP
Total Poisoning cases in 2014 = 254
Organophosphorus poisoning = 55
In 2015, 7 cases reported till date
1 death reported in 2015
1 case currently admitted in RRRML Data
Why is OP poisoning common ??India is an agrarian
countryroutinely used in farming
CAUSES OF HIGH MORTALITYHigh toxicity of available compoundsTime
gap in transporting patientsPaucity of Health care personnelLack of
training facilitiesLack of antidotes
Why is OP poisoning common ??
Limited resources and infrastructure for health care
delivery
1. Mode of poisoning* Banerjee I, Tripathi SK, Roy AS.
Clinico-Epidemiological Characteristics of Patients Presenting with
Organophosphorus Poisoning. N Am J Med Sc. Vol 4(3), JMarch
2012
2. Occupation* Maharani B, Vijayakumari M. Profile of poisoning
cases in a tertiary care hospital in Tamil Nadu, India. J of App
Pharma Sc. Vol 3(01), Jan 2013
3. Seasonal distribution* Maharani B, Vijayakumari M. Profile of
poisoning cases in a tertiary care hospital in Tamil Nadu, India. J
of App Pharma Sc. Vol 3(01), Jan 2013
4. Type of Poison* Banerjee I, Tripathi SK, Roy AS.
Clinico-Epidemiological Characteristics of Patients Presenting with
Organophosphorus Poisoning. N Am J Med Sc. Vol 4(3), JMarch
2012
5. Relative human Toxicity
Eddleston M et al. Differences between organophosphorus
insecticides in human self-poisoning: a prospective cohort study.
Lancet. 2005 Oct 22-28;366(9495):1452-9
Mechanism Of Action
Clinical Features1. Acute O-P poisoning- Muscarinic features
Resp distress- Nicotinic features Death- CNS features
2. Intermediate Syndrome
3. Delayed neuropathy (OPIDP)
4. Neuro-psychiatric disorder (COPIND)
1. Acute O-P poisoningMUSCARININC FEATURESNICOTINIC FEATURESCNS
FEATURES D iarrhoeaMuscle weaknessFatigue U rinationMuscle
fasiculationsConfusion M iosisMuscle paralysisUnconsciousness B
ronchorrhea B ronchospasmSeizues E mesisHypertensionAtaxia L
acrimationTachycardiaResp. depression S alivation S weating
2. Muscarinic / Wadia type 1 syndrome
1. Excessive Sweating2. Miosis3. Bronchorrhoea / spasm4.
Bradycardia
5. Hypotension
3. BronchorrhoeaEarly cause of morbidity and mortality
Excess fluid is from airway secretions
Obstruction of upper and lower airways
Pulmonary edema - - hypoxia - - death
The Grading of Clinical severity
4. Intermediate syndromeDescribed in 1987 (Karalliedde and
Senanayake)
Occurs 24-96 hours after resolution of acute cholinergic
crisis
Most imp. factor responsible is quantum of exposure of OPC
May occur from inadequate oxime therapy
IMS - pathophysiology Incidence = 10-50 %
Prolonged effects on Nicotinic receptors
Primary motor end plate degeneration
Leads to muscle weakness
IMS- muscle weakness ofMuscles innervated by cranial nerves :
III-VII and X
Neck flexors- a constant feature- one of the earliest signs -
inability of patients to raise heads off pillow
Proximal limb muscle weakness- typically involve shoulder
abductors, hip flexors
Respiratory muscles - death
IMS other featuresDeep tendon Reflexes :Usually absent /
decreased Sensory system usually intact
Muscarinic symptoms :absentrarely short relapses may occur
IMS- complicationsWeakness -- Frank paralysis
Respiratory distress -- Death
Main cause of morbidity and mortality in Indian patients.
25
5. OPIDPOP induced Delayed Polyneuropathy
Delayed, rare, neurotoxic effect
1-5 weeks after severe acute poisoning, due to slow release of
OP from body fat
symmetrical sensory-motor axonal degeneration of the peripheral
nerves and SC
5. OPIDP - C/fMotorSharp cramp like pain in calfHigh stepping
gait (initially)Shuffling gate in severe casesQuadriplegia /
paraplegiaWrist and foot dropMild pyramidal signs
SensoryGlove-stocking anesthesiaCerebellar signs +/-
6. COPINDChronic OP induced Neuro-psychiatric disorder
Chronic low-dose exposure to OP compounds
40 hours/week, 9 months/ year
No cholinergic symptoms
Non responsive to levodopa
Plasma cholinesterase levels are normal
6. COPIND c/fNeurological SymptomsPsychiatric Symptoms1.
Impairment in memoryAnxiety2. Impairment in
concentrationDysthymia3. Impairment in leaningDepression4. Chronic
fatigue5. EPS : dystonia6. Resting tremor, bradykinesia7. Rigidity
of face Parkinson-like8. Postural instability
Non responsive to levodopa
Diagnosis and Management
Diagnosis of OP poisoningDiagnosis is mainly clinical, Based on
:
H/o Ingestion of poisonCharacteristic clinical featuresClinical
improvement after atropine/ oximeReduction of cholinesterase
activity.
1. Inhibition of cholinesteraseDemonstrating a decrease in
cholinesterase
Definitive or gold standard method
Theoretically RBC/ true cholinesterase is more accurate than
plasma/ pseudo
But plasma / pseudo-cholinesterase is more easily available
test
Diagnosis :Plasma / SChE : - easy to measure- easily available-
more useful in acute exposure
50 % reduction in normal values : diagnostic (baseline values
usually NA)
Progressive increase in SChE with treatment
2. Cholinesterase levelsUseful in monitoring clinical course of
illness
persistent Low levels are a predictor of IMS (Intermediate
syndrome)
SChE activity is < 20 % during onset of IMS* Tajune J, Robert
J. Organophosphoric poisoning. Ann Emerg Med 1987 ; 16:193.
Drawbacks of Cholinesterase assays.Plasma Butyrylcholinesterase
assayNo info about clinical severity.Produced by liver, recovery
about 7% of normal each day, so can only guide in recovery and not
specifically the poisoning.Variations in commercial assays.Temp.
control is required. (Activity increase with 1o C increase)
Red cell acetylcholinesterase assayEnzyme and OP compounds
continue to react in blood sample at room temp.Blood sample :
Dilute with factor of 20. (200 L fresh blood into EDTA tube mix 4ml
cold saline (4o C) place in freezer at 20 oC within 5 min.Sensitive
to concentration of oxime, and substrate and pH. So low substrate
conc, at pH7.4 will reduce accuracy.
3. Electro-neuro-myogram (ENMG)
30 Hz rapid nerve stimulation - decremental responses correlate
best with clinical weakness
Most useful diagnostic test of IMS ** Senanayake N et al.
Neurotoxic effects of OP insecticides : an intermediate syndrome.
NEJM. 1987 ; 316 :761-63.
4. Other tests of prognostic valueHyperglycemia Neutrophilic
leucocytosisProteinuria / glycosuriaECG changes (QTc
prolongation)Blood pH (acidosis)Hyper amylasemiaSerum CPK
levels
5. Hyperglycemia in OP-poisonOxidative stressRenal tubular
damage Stimulation of adrenalsRelease of catecholamines
Transient hyperglycemia and glycosuria are often seen in acute
OP-poisoning * Namba T, Nolte CT, Jackrel J, Grob D. Poisoning due
to organophosphate insecticides: Acute and chronic
manifestations.Am J Med.1971;50:47592.
6. Blood pHMetabolic Acidosis develops in patients of OP
poisoning, more common with hypotension*1.
Unknown mechanism. If pH < 7.20, treatment with sodium
bicarbonate beneficial*2.
*Prakash O.et al. Low ph predicts mortality in OPP and
carbamates poisoning, JAPI 2002; 50:857.*Roberts DM, Buckley NA.
Alkalinisation for treating organophosphorus pesticide poisoning.
Cochrane Database of Systematic Reviews 2005;1:CD004897.pub2.
7. QTc prolongationIndicates poor prognosis in OP- poisoning
1. Cholinergic stimulation of heart : M2a. negative ionotropyb.
negative chronotropy
2. Oxidative stress causes conduction problems
* Shadnia S, Okazi A, et al. Prognostic value of long QTc
interval in acute and severe OP poisoning. J of Med Toxico 2009 ;
5(4).
8. Hyper- amylasemiaCholinergic stimulation of salivary
glandsCholinergic stimulation of pancreasAcute pancreatitis
(rare)
Raised amylase levels correlate with severity and presence of
shock in acute OP poisoning *
* Lin CL, Yang CT, Pan KY, Huang CC. Most common intoxication in
nephrology ward organophosphate poisoning. Ren Fail 2004
;26:349-54..
9. Acute Pancreatitisd/t Excessive cholinergic stimulation and
ductular hypertension
Painless Ac. Pancreatitis has been reported
Amylase (>300) : low Sn, low SpLipase (>300) : useful for
diagnosis* Hsiao CT, Yang CC, Deng JF, Bullard MJ, Liaw SJ. Acute
Pancreatitis following Organohosphate Intoxication. J Toxicol Clin
Toxicol. 1996 ;34(3):343-7.
Management
What to do ??Call AIIMS poison cell : (NPIC)
- National Poisons Information Cell - Toll free no. 1800 116
117- Other : 011 - 26589391- Open 24 X 7 , 365 days a year
1. Identification of poisonHistory by patient/ attendantClinical
presentation.By showing photographs.WHO colour code on
container.
Poison :Identification
WHO colour code on container.Red labelExtremely
toxicMonocrotophos,zinc phosphide,ethyl mercury acetate, and
others.Yellow labelHighly toxicEndosulfan,carbaryl,quinalphos,and
others.Blue labelModerately toxicMalathion,thiram,glyphosate,and
others.Green labelSlightly toxicMancozeb,oxyfluorfen, mosquito
repellant oils and liquids, and most other household
insecticides.
46
Identification of poisonSigns of cholinergic excess or
developing intermediate syndrome Disparity between history and
clinical presentation, follow, clinical judgment.After
identification classify as Organophosphorus and
non-Organophosphorus.
Organophosphosphate
Management :Immediate, Protocol
When not sure about the poison..??Atropine test : Inject 0.6- 1
mg IV atropine.If pulse rate goes up by 25 per minute or skin
flushing develops patient has mild or no toxicity for OPs.
Management : SpecificGeneral Principles of Therapy :
Decontamination, Resuscitation, Stabilization.Muscarinic
antagonistsFluids.Acetylcholinesterase reactivators.Gastric
Decontamination.Miscellaneous.
DecontaminationHealthcare workers and OP Poisoning.Few western
hospitals, reported such poisoning.None shows inhibition of
Acetyl/Butyryl cholinesterases.Cases from Asia : Health-care
workers take no special precautions , No cases of secondary
poisoning reported.
Decontamination
Guidelines : Universal Precautions, Maximum Ventilation,
Frequent rotation of staff to keep exposure minimum.PPE should not
consist Latex / Vinyl.Patient : All clothing to be removed, discard
in ventilated area.Thorough irrigation with water.Wash with soap
and water.Soaps containing 30% ethanol advocated.Ocular
decontamination : water only.
Initial Stabilisation
Patent Airway, adequate Breathing and Circulation.Oxygen at
first opportunity.Little evidence, Atropine not to be given until
oxygen availability*1. However, in hospitals where oxygen not
available, Atropine to be started early*2.Patient Position : Left
Lateral, Neck Extended.Reduce aspiration risk.Keeps airway
patent.Decrease pyloric emptying and absorption of poison.*1Erdman
AR. Insecticides. In: Dart RC, Caravati EM, McGuigan MA, et al,
eds. Medical toxicology, 3rd edn. Philadelphia: Lippincott Williams
& Wilkins, 2004: 147596.
*2Aaron CK. Organophosphates and carbamates. In: Shannon
MS,Borron SW, Burns M, eds. Clinical management of poisoning and
drug overdose, 4th edn. New York, Elsevier Science, 2006.
Initial Stabilisation
Gastrointestinal decontamination
Often first intervention
To be considered only after stabilization, oxygen, atropine and
oximes.Lavage only if patient arrives within 1 hour.Only consider
if patient intubated or conscious and willing to cooperate.* The
Hazards of Gastric Lavage for Intentional Self Poisoning in a
Resource Poor Location Clin Tox 2007;45(2):136-43
Not beneficial, rather increases chances of Aspiration Pneumonia
& Deaths*
Gastrointestinal decontaminationInduced emesis : Ipecacuanha
induced , Contraindicated.Activated charcoal : Studies failed to
find any benefit ( Why..??)It binds in vitro, but not in gut due to
rapid absorption.Ingested dose too large for the amount of
charcoal. * Eddleston M, Juszczak E, Buckley NA, et al. Randomised
controlled trial of routine single or multiple dose superactivated
charcoal for self-poisoning in a region with high mortality. Clin
Toxicol 2005; 43: 44243.
Gastrointestinal decontaminationInduced emesis : Ipecacuanha
induced , Contraindicated.Activated charcoal : Studies failed to
find any benefit ( Why..??)It binds in vitro, but not in gut due to
rapid absorption.Ingested dose too large for the amount of
charcoal. NO evidence suggests that patients with pesticide
poisoning benefit with activated charcoal.** Eddleston M, Juszczak
E, Buckley NA, et al. Randomised controlled trial of routine single
or multiple dose superactivated charcoal for self-poisoning in a
region with high mortality. Clin Toxicol 2005; 43: 44243.
Muscarinic antagonist
Muscarinic antagonist
A small RCT found no difference in mortality or ventilator
rates, comparing Atropine and Glycopyrrolate.Hyoscine : best for
severe Extra-pyramidal features with few peripheral signsIn animal
studies, found more effective than Atropine for control of seizures
induced by inhaled nerve gas agents.However, Atropine remains
mainstay of therapy.Easy and wide availability.Affordability
.Moderate ability to penetrate CNS.
Muscarinic antagonist
AIM OF THERAPY : ATROPINETo reverse cholinergic features.To
improve Cardiac and Respiratory functions.Target Endpoints of
Atropinization.Drying of Pulmonary secretions, ie. Clear lung
fields on auscultation. (Most reliable)Heart rate > 80 beats /
min.SBP > 80 mmHg.Pupils : No longer pinpoint.Dry Axillae.Bowel
sounds : just present.
End points of atropinisation
Lung secretionsHypotensionBradycardiaSweatingMiosisBowels :
Hyperactive
ATROPINEClear ChestSBP > 80mmHgHR > 80/minDry
AxillaePupils no longer pinpoint.Bowel sounds : Just present
Atropine Dosing
Incremental Dosing
1.8 to 3 mg Atropine (i/v)Repeat every 5 minutes with doubling
the dose each time.Endpoint : Atropinization.Followed by : 10 to 20
% of total dose required for atropinization every hour via i/v
infusionTo be held once anticholinergic effects occur.(Absent bowel
sounds, urinary retention, agitation).Bolus DosingV/S2-5 mg
Atropine every 10 to 15 min.
Endpoint : Atropinization.Followed by maintenance using reduced
doses or increasing time duration in b/w doses.
Atropine Dosing
Incremental Dosing
1.8 to 3 mg Atropine (i/v)Repeat every 5 minutes with doubling
the dose each time.Endpoint : Atropinization.Followed by : 10 to 20
% of total dose required for atropinization every hour via i/v
infusionTo be held once anticholinergic effects occur.(Absent bowel
sounds, urinary retention, agitation).Bolus DosingV/S2-5 mg
Atropine every 10 to 15 min.
Endpoint : Atropinization.Followed by maintenance using reduced
doses or increasing time duration in b/w doses.
Various studies clearly found Incremental Dosing far superior to
bolus dose administration
Atropine Monitoring
Patient to be assessed every 15 min to check adequacy of
dosages.If clinical features recur, further increment in boluses
and doubling.Once parameters reached, Monitoring hourly for atleast
6 hours to check effectiveness of infusion.
Timeheart rateClear lungPupilDry axillaSBP > 80 mm HgBowel
soundsmental stateFever >37.5cSPO2Atropine infusion dose
OP / Carbamate Observation Sheet
Atropine : When to stop..??
Bronchorrhoea : most important, for titrating dose. Atropine
toxicity = absent bowel sounds + fever + confusion.Stop infusion
for 60 min, if toxicity.Re-start infusion at 80% of initial rate,
once the temp. comes down and patient calms.Most do not need
>3-5 mg (5-9 ml) / hour of atropine infusion.Reduce rate by 20%
every 4 hourly once patient is stable. STOP.
OximesReactivate Acetyl cholinesterase, remove phosphoryl
group.Discovered in 1950s by Wilson et al.Among various oximes
(obidoxime and trimedoxime) Pralidoxime (PAM) remains, most widely
used.Prevent continued toxicity by Scavenging and detoxifying
enzyme.Also endogenous anticholinergic effects.Available in four
Salts : chloride, iodide, metilsulfate, and mesilate.Chloride and
iodide most widely used in developing countries.Chloride salt
better than iodide.More active compound per gram of salt.No risk of
thyroid toxicity.
OximesTherapeutic effectiveness depends onConcentration of
poison consumed (Poison load).Time lapse between poisoning and
administrationType of OPC. (More effective on diethyl than
dimethyl). Dimethyl compound reactivate and age at slower
rate.Lipid solubility of OPC.Concentration of Oxime in blood.
OximesThe ControversiesTwo RCTs in Vellore, India in early 1990s
noted, Harm from low dose PAM infusion.A Cochrane review ( included
two RCTs , 2005) & two other meta-analysis reported no clear
benefit or harm.An RCT in Baramati, India studying very high dose
of PAM in 200 patients with moderate OP poisoning showed reduced
Case fatility. (1% vs 8%).
OximesThe consensusOximes will not be effective in very severe
(large dose) poisoning.Treatment with oximes should be started as
early as possible, no role if started after 48 hours.Less effective
in severe complications such as aspiration pneumonia or hypoxic
brain injury before treatment.Less or no effectiveness with
dimethyl compounds and atypical organophosphates.Not effective in
carbamates but are not contraindicated either*.*Carbamate
poisoning: treatment recommendations in the setting of a mass
casualties eventAm J Emerg Med.2009 Nov;27(9):1117-24. doi:
10.1016/j.ajem.2009.01.035
OximesDosingPAM : 1-3 gm/day, no role after 48 hrs.Serum levels
of > 4 mg/lit is necessary for effective treatment.To achieve
this, administered as bolus 20-40mg/kg followed by continuous
infusion at 500mg/hr.WHO recommendations : Loading dose 30mg/kg,
followed by infusion of 8mg/kg/hr.
OximesTherapeutic end pointResolution of muscle fasciculation
and weakness, Reactivation and Increment in SChE levels.Use longer
than 24 hours indicated if unaged OPs release from fat
tissue.Infusion continued until patient remains symptom free for
atleast 12 hours without additional atropine.Or until
extubated.
Role of BenzodiazepinesControl agitation.Sedation in ventilated
patients.Many opioids, metabolized via SChE, so use for sedation in
pulmonary edema can worsen CNS manifestation.Control of seizures :
First line therapy in OP poisoning, phenytoin not recommended d/t
membrane stabilizing effects.Seizures uncommon in oxygenated
patients, more common in nerve gas agents (soman and
tabum).Diazepam reduce neural damage and prevent respiratory
failure (animal studies).
Role of Magnesium Sulphate
MgSO4 (4g) i/v in first day after admission, decrease
hospitalization period and mortality.It blocks Calcium channels and
reduce acetylecholine release from presynaptic terminals.Also
reduces CNS overstimulation from NMDA receptor activation.
Role of ClonidineCentrally acting 2-adrenergic receptor
agonists.Reduces acetylcholine synthesis and release from
presynaptic terminalsAnimal studies, shown benefit in combination
with atropine. Effect in humans unknown.
Advanced Neuroprotective Drugs
Ketamine : Noncompetitive NMDAR antagonist, within 1 hour of
nerve gas agent induced seizures along with
Midazolam/diazepam.Tezampanel : Glutamate receptor antagonist
specific for kainate subtype Rc, useful in soman(nerve gas) induced
seizures and neuropathy.Gacyclidine : Another antiglutamatergic
compound found beneficial in conjunction to standard therapy in
nerve gas poisoning .
Advanced Neuroprotective Drugs
For OPIDN : standard therapy plus corticosteroids.Protease
inhibitors : target esterase and prevent delayed
neuropathy.Intermediate syndrome resistant to standard treatment,
artificial respiration.Antioxidants : lipid peroxidation and
thiobarbituric formed in OP poisoning, Antioxidant beneficial.
Vitamin E reported to have therapeutic effect
Intermediate syndrome : ManagementUsually presents 12 to 96
hours after exposure.Early signs : action tremors and pharyngeal
weakness (difficult deglutition , pooling of secretions).Later :
inability to flex neck, DTRs lost, cranial neuropathies, proximal
muscle weakness and respiratory muscle paralysis.Not all require
intubation and ventilation, but patients with tremors and
pharyngeal weakness, at increased risk.Treatment : totally
symptomatic. Ventilator support if respiratory muscle
paralysis.
Ventilatory SupportIndicated in stupor / coma, Hypoxemia (PaO2 5
mL/kg at Pressure of 3-5 cm of H2O.
Parameter Weaning thresholdPaCO2 20 L/minRespiratory frequency 6
breaths/min
Role of AlkalinizationIV infusion of Soda. Bicarbonate produce
moderate alkalinization (pH : 7.45 to 7.55) in OP
poisoning.Infusion of higher dosages (5mEq/Kg) in 60 minutes
followed by 5-6 mEq/kg/day was shown useful.(In dogs)More
beneficial in Nerve agent poisoning.Cochrane review : Insufficient
evidence to establish use of NaHCO3 in human OP Poisoning.
Role of Early Enteral Feeding. Early enteral feeds associated
with improved outcomes in critically ill because it prevents
enterohepatic circulation.Early nutritional supplementation in OP
poisoning assumes importance as these patients may require
prolonged ventilatory support.
Role of Fresh Frozen Plasma. FFP contains important components
like clotting factors, proteins, enzymes, etc.It is hypothesized
that butyrylcholinesterase present in FFP sequester free poison in
blood and remove it from circulation.Two trials, both unfavourable
to FFP intervention.
Role of Fresh Frozen Plasma. FFP contains important components
like clotting factors, proteins, enzymes, etc.It is hypothesized
that butyrylcholinesterase present in FFP sequester free poison in
blood and remove it from circulation.Two trials, both unfavourable
to FFP intervention.Current evidence not strong enough to make
clear conclusion regarding bioscavenger role of FFP
For the future..Removal of OPs from blood : Hemodialysis,
Hemoperfusion or hemofiltration.Hemofiltration after dichlorovos
poisoning revealed beneficial therapeutic effects.Military research
aims at : Injecting Butyrylcholinesterase after cloning into
soldiers before exposure to nerve gases.Not practical for
prophylaxis in self-poisoning as one cannot predict when a person
is going to ingest pesticide.Use of recombinant bacterial
phosphotriesterases, or hydrolases to break down OPs
enzymatically.
Take home messageEarly stabilization and resuscitation.
Incremental dose Atropine.Early institution of Oximes.External
decontamination, MgSO4, Clonidine, Use of benzodiazepines and NMDA
receptor antagonists, Alklinization, Early Enteral feeding were
found to be beneficial.FFP, forced emesis were found
harmful.Activated charcoal, Gastric lavage were found to have no
benefit or harm.Gastric lavage : easily performed, cheap could be
used as an adjunct if performed within one hour.
Thank You
SeverityAChE
(RBC)MuscarinicNicotinicCNS
Mild> 40%nausea, vomiting, diarrhoea, salivation,
bronchorrhoea and -constriction, bradycardia
headache, dizziness
Moderate 20 - 40%as above, + miosis, incontinencefasciculations
(fine muscles)as above, + dysarthria, ataxia
Severe< 20%as above, + fasciculations (diaphragm, resp.
muscles)as above, + coma, convulsions