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: Harrisons 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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Refractory Seizure
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.

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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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PARAQUAT POISONING
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

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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
GIT ulceration

Vomitiing

Ingestion

Burning sensation of GIT

Abdominal pain

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Inhalation

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Multisystem Failure
GIT corrosion, perforation and haemorrhage Acute tubular necrosis and Renal failure Hepatocellular necrosis and Hepatic failure

Congestive heart failure

Pulmonary oedema and Pulmonary fibrosis

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Chest Radiograph

Diffuse consolidation indicating Parenchymal injury

Pneumomediastenum

Pneumothorax Corrosive rupture of oesophagus

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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 A&E(VINAYAKA)

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%
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Toxicity of Glyphosate

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
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On Ingestion Local effects

Nausea Vomiting Diarrhea

Oesophageal corrosion

Gastric ulcer

Pulmonary edema

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On Ingestion Systemic effects

Hepatic impairment Reduced organ perfusion Renal impairment

Hypotension

Myocardial depression
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Broad complex tachycardia Ventricular arrhythmia

ECG Changes

Bradycardia
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Dilated pupil

CNS Effects

Confusion

Deep coma Convulsions

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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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Severe Toxicity

Loss of consciousness

Recurrent convulsions

Cardiac arrest

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Old Age

High Concentration

Chest infiltrates

Prognostic Factors
Shock Arrhythmia

Dialysis

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Pulmonary Edema

Mortality Triad

Hyperkalemia

Metabolic Acidosis
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Management

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Management

Symptomatic

Supportive

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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
Breath test
Filter paper impregnated with 0.1N silver nitrate Patient is asked to breathe through it for 5 to 10min Filter paper turns black
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Biological sample test

5 to 10ml of gastric aspirate is added to equal amount of water + HCl Heated upto 50 * C for 15 minutes Silver nitrate filter paper is dipped Turns black
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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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Aluminum Phosphide
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.
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