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

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Reduced organ perfusion Renal impairmentHepatic impairment

Myocardial depression

Hypotension

On Ingestion – Systemic effects

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ECG Changes

Broad complex tachycardiaVentricular arrhythmia

Bradycardia

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CNS Effects

Emergency Medicine

Dilated pupil Confusion

ConvulsionsDeep coma

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Inhalation toxicity is fatal due to rapid systemic absorption

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Renal failure requiring dialysis

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Consider in Resistant Hypotension And Acidosis.

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Respiratory insufficiency requiring intubation

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Recurrent convulsionsLoss of consciousness Cardiac arrest

Severe Toxicity

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Prognostic Factors

Old Age High ConcentrationChest infiltrates

ArrhythmiaShock

DialysisLOC

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Mortality Triad

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Management

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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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