Dr v P Chandrasekaran

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Pesticide Poisoning – What is new?

Dr.V.P.Chandrasekaran.

M.D., Diploma in Accident & Emergency Medicine

Head. Department of Emergency & Critical care Medicine

Vinayaka Missions Kirupananda Variyar Medical College

Salem

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Poisoning – A global Threat

• Suicidal attempts

• Accidental and occupational exposure to poisons.

• South Asia - Agriculture

• Pesticides – Multipurpose

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Objective

• Newer aspects and controversies

– Organo phosphorous compounds

– Organo chlorine

–Pyrithrines and pyrithrinoids

– Glyphosate

–Aluminum Phosphate

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Organo phosphorus

• Muscular paralysis

• Secretions

• Needs supportive care like Airway, ventilation and treated with charcoal, Atropine and oximes

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Charcoal - Controversies

• Questionable value

• Harmless when handled carefully

• GI obstruction – prevent with Hydration

• Aspiration – Protect airway when in need

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Why Multi dose Activated Charcoal for 48 hrs?

• Direct Adsorption

• Enterohepatic circulation

• Gut Dialysis

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What is new?

• Hypokalemia - needs close monitoring when MAC given.

• Never been reported so for and it is lethal when unnoticed and not corrected

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Atropine

• What is the end point?

–Dilation of pupil and tachycardia are not the real end point

–The real end point of atropinisation should be the drying of secretion.

• Harms – Delerium, Gastro peresis

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Tracheobronchial secretions

Ref: Tintinalli 6th edition

Ref: Harrison’s 17th edition

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How to prevent Delirium?

• The Glycopyrolate can be added to atropine to reduce the delirium as it will not penetrate the blood brain barrier and dry the secretions

• Glycopyrolate should not be used alon as it does not counter th CNS effects of poison

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oximes• Questionable value

• Incidence of Asystole and type 2 respiratory failure is reported

• It is believed harmful by many clinicians.

• Require multicentre studies to clear the dilemma.

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Less Known• OPC induced Parkinsonism

• Malignant neuroleptic syndrome (tremor, rigidity, hyperthermia and increased CPK).

• Precipitated by metaclopromide Needs high index of suspicion, early recognition

and meticulous attention to save the patient.

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Better Outcome

• Magnesium sulphate

• Soda bicarbonate infusion to keep the pH of 7.45 -7.55

it needs to be addressed by researchers seriously.

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Pyrithrines and Pyrithrinoids

• Less lethal poisoning (drowsiness, seizures and the seizures) can be countered by lorazepam and phenobarbitone.

• In combination with OPC - lethal and the incidence of ARDS seen more after this poisoning.

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Organo chlorines

• More dangerous and characterized by refractory seizure (Endosulphan).

• But the newer protocol devised by Vinayaka missions university emergency physicians is promising in saving life.

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Why to intubate electively?

• There will be no aura before the onset of convulsion hence it is mandatory to electively intubate all the patient even when their GCS is 15/15 ( As the airway needs to be protected in refractory seizures).

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Why no Charcoal with out intubation?

• Charcoal should never be instilled unless the intubation is done as the possibility of aspiration when seizures begin with out aura.

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Seizure control

• Phenytoin – No role in seizures secondary to poisoning.

• Though lorazepam and Phenobarbitone –not adequate

• Thiopentone infusion gives good control.

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Refractory Seizure

• Intermittent neuromuscular blocking agents prevent renal failure, hyperkalemia, acidosis and rhabdomyolysis secondary to refractory seizure.

• Episodes of seizures are indirectly reflected as salivation and papillary changes. But bed side EEG monitoring will help us better.

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• Propofol not preferred as propofol infusion syndrome is more when it is used >4mg/kg/hr along with Vasopressors, steroids (Rhabdomyolysis, fever, acidosis and hypotension ). Hence it is not used widely.

•

Refractory Seizure

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Shock management

• Toxin induced cardiac suppression

– Dopamine and Nor Adrenaline

• Central venous catheterization and CVP guided fluid is mandatory.

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Steroids

• Sudden death is possible due to malignant cerebral edema; the role of steroid is not studied. But in our center we are using when no significant contra indication is noted.

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No early declaration of Brain Dead

• Thiopentone coma may continue for days together due to cumulative effect of the Thiopentone when used more ( up to 10 days)

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• Herbicide , Belongs to Bipyridyl group• Severe local irritant and devastating Systemic

toxin• Manufactured – liquids, aerosols & granules• Ingestion – systemic toxicity and deaths• Inhalation - unlikely to cause systemic toxicity

PARAQUAT POISONING

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Acute Exposure

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Toxic Dose

• Ingestion of <20mg/kg - Moderate GI symptoms

• 20-40mg – Results in death from 5th day to several weeks

• >40mg – Usually die within 1-5days

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Clinical Features

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Inhalation

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Multisystem Failure

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Chest Radiograph

Pneumomediastenum

Pneumothorax Corrosive rupture of oesophagus

Diffuse consolidation – indicating Parenchymal injury

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Upper GI Endoscopy

Erosions Ulcers

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Treatment

• ABC

• Low inspired O2 (prevent superoxide radical formation with the goal of reducing pulmonary injury)

• Early and vigorous decontamination• Multi dose activated Charcoal• Steroids• Antioxidents

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What is new?

• Charcoal Haemoperfusion: Instituted as soon as possible and continue Q6H

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What is new?

Plasma Exchange – aggressive , multiple cycles with in 24 hours is promising in saving life

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Glyphosate

• N-phosphonomethyl glycine

• Phosphorous containing organic compound

• A post emergent Herbicide

• Surfactant toxicity

• Concentrations range from 1-41%Emergency Medicine

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Toxicity of Glyphosate

Emergency Medicine

Enhance ATPase Activity

Uncouples Mitochondrial Oxidative phosphorylation

Toxicity of Surfactant

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Factors contributing Toxicity

• Type & concentration of the surfactant

• Salt partner & other adjuvants

• Severe human poisoning 41% glyphosate isopropylamine & 15% polyoxyethylene amine

Emergency Medicine

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NauseaVomiting Diarrhea

Oesophageal corrosion Gastric ulcer Pulmonary edema

On Ingestion – Local effects


Reduced organ perfusion Renal impairmentHepatic impairment

Myocardial depression

Hypotension

On Ingestion – Systemic effects


ECG Changes

Broad complex tachycardiaVentricular arrhythmia

Bradycardia

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CNS Effects

Emergency Medicine

Dilated pupil Confusion

ConvulsionsDeep coma


Inhalation toxicity is fatal due to rapid systemic absorption

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Renal failure requiring dialysis

Emergency Medicine


Consider in Resistant Hypotension And Acidosis.


Respiratory insufficiency requiring intubation


Recurrent convulsionsLoss of consciousness Cardiac arrest

Severe Toxicity


Prognostic Factors

Old Age High ConcentrationChest infiltrates

ArrhythmiaShock

DialysisLOC


Mortality Triad

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Management

Emergency Medicine


Management


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Aluminium & Zinc Phosphide

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Aluminium Phosphide Celphos , Quick pos ,Phosfume

Greyish - white tablets, 3gm each

Garlicky Odour

Fatal dose: 1-3 tablets

High mortality.

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Aluminium phosphide

Filter paper impregnated

with 0.1N silver nitrate

Patient is asked to breathe

through it for 5 to 10min

Filter paper turns black

Breath test

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Silver nitrate test

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Aluminum Phosphide

• Immediate consumption of oil reduces the release of phosphin gas and reduces the complication.

• Water lavage is contraindicated as it can increase the release of phosphin Gas.

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• IABP, Glucose Insulin Potassium infusions , sodium bicarbonate infusion have been used to treat this poison but the outcome is variable and these are not always helpful.

Aluminum Phosphide


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Dr v P Chandrasekaran