Crashing Patient

  • Home
  • EMCrit Blog
  • Index
  • Contact
You are here: Home / 14. Toxicology / Pesticides, Herbicides and Rodenticides

Pesticides, Herbicides and Rodenticides

July 14, 2011 by CrashMaster

Pesticides

Organophosphates

Block ACh-esterase

SLUDGE

Diarrhea, diaphoresis

Urination

Miosis

Bradycardia, bronchosecretions, bronchostriction

Emesis

Lacrimation

Salivation

Nicotinic effects can give mydriasis, fasiculations, and paralysis

Confusion and coma

Can be brady or tachycardic

Strong Rancid Odor, Garlic-like

Some labs can run cholinesterase levels, get plasma and RBC (for chronic intox)

 

Decon-can penetrate latex, use rubber gloves

Supportive Rx

Atropine (for muscarinic effects) 5mg IV Q5 minutes until control of mucosal secretions

May need up to 500 mg in the first hour, followed by 100 mg per hour\

better method is to start with 3 mg and double every 5 minutes until desired response (J Med Toxicol 2012;8:108-117.)

Pralodoxime (2-Pam)

1-2 grams (25–50 mg/kg) IV over 15 minutes, then 500 mg/hr.  Must be given early as once acetylcholinesterase ages, 2-Pam will not work.  Can cause arrest if given rapidly.

Cont infusion is better Lancet. 2006 Dec 16;368(9553):2136-41. FINDINGS: 100 patients were assigned the high-dose regimen, and 100 the control regimen. There were no drop-outs. Patients receiving the high-dose pralidoxime regimen required less atropine during the first 24 h than controls (median 6 mg vs 30 mg; difference 24 mg [95% CI 24-26, p<0.0001]). 88 (88%) and 64 (64%) of controls and high-dose patients, respectively, needed intubation during admission to hospital (relative risk=0.72, 0.62-0.86, p=0.0001). Control patients required ventilatory support for longer (median 10 days vs 5 days; difference 5 days [5-6, p<0.0001]). INTERPRETATION: A high-dose regimen of pralidoxime, consisting of a constant infusion of 1 g/h for 48 h after a 2 g loading dose, reduces morbidity and mortality in moderately severe cases of acute organophosphorus-pesticide poisoning.

Intermediate Syndrome:  It occurs after initial symptoms of cholinergic excess have resolved, but before the development of delayed peripheral neurological deficits that may take days or weeks to occur, thus the name “Intermediate Syndrome”

Carbamate Insecticides

Same as organophosphates, but only last a few hours. May not need 2-Pam as they bind AChase reversibly, but probably still safer to give as only animal studies exist.

Chlorinated Hydrocarbons

DDT, Lindane, etc.

sensitize heart to catecholamines, seizures

Pyrethrins and Pyrethroids

Permethrin, cypermethrin, deltamethrin, fenvalerate

Can cause paresthesias, allergic rxns, coma, fasiculations, seizures, NCPE

Decon and supportive care

Nicotine

Green tobacco sickness gi sx, HA, dizziness, and diaphoresis.

Deet

Seizures, coma, neurotoxicity.  But remarkably safe considering widespread use.

Substituted Phenols

uncouple oxidative, can cause hyperthermia

Pyrimidifen Intoxication (Annals EM 42:2, 2003)

some similarities to organophosphates.    Causes circulatory shock.  At this point, only symptomatic treatment can be offered.

Herbicides

Paraquat

used to spray marijuana fields, activated by sunlight, inactive by burning, harvest at night and your crop is still good.

Highly tissue toxic

Direct pulmonary destruction

GI ulcers and possible esophageal rupture

Acute renal failure from proximal tubule destruction

Free radical formation

 

Aggressive orogastric Lavage in first 1-2 hours even if asymptomatic

AC

Avoid O2 if possible to decrease free radicals

Fullers Earth to inactivate unabsorbed paraquat

Use charcoal hemoperfusion

Consider pulse steroids and cyclophosphamide

Diquat

Similar ot above in presentation and management, but need higher doses to be toxic

Chlorphenoxy Acids

agent orange

Nausea, diarrhea, abd pn, ataxia, paralysis, coma, rhabdo

Rodenticides

Aldicarb

Tres pasitos (three steps), illegally imported from the DR

Carbamate poisoning

 

 

Red squill

Arsenic

Thallium, tetramine

Strychnine, sodium monofluoroacetate (compound 1080)

Barium, bromethalin

Phosphides, phosphorous (yellow or white), PCNU

Arsenic

Norbormide

Indanediones

Coumadin-like anticoagulants

 

Red Squill

cardiac glycoside from sea onion. Very powerful emetic so most ingestions self-decontaminate

 

Alpha-napthyl thiourea (ANTU)

Increases capillary permeability in the lungs

Dyspnea, rales, NCPE

No antidote

 

TETS

tetramethylenedisulfotetramine

called dushuqiang in china

severe seizures

odorless, tasteless water soluble powder

gaba antagonist, irreversibly binds

lethal dose 7-10 mg

also consider thallium which can present with gi symptoms, alopecia and neuropathies

Strychnine

Nausea, usually without vomiting

Muscle hyperexcitability, hyperreflexia, convulsions without loss of consciousness

Benzos, supportive care

 

PNU (Vacor )

Kills pancreatic beta cells

Causes DKA

Treat with niacinamide, no longer available IV, po at supplement stores

 

Arsenic trioxide

heavy metal which causes gi symptoms and cardiovascular collapse

 

Norbomide

stimulates rat-specific smooth muscle receptor causing intense vasoconstriction

not toxic to humans

 

Indanediones

substances such as chlorphacinone and pindone are non-coumadin anticoagulants

 

Coumarins

Superwafarins

Inhibits vit k dependant activation of factors II,VII,IX,X by preventing regeneration of Vit K.

Bleeding

AC

Vitamin K1 (not K3)

Consider FFP

In kids, get a baseline PT, if normal bring them back in 48 hrs for repeat.  If normal, you are done.  If abnormal then give Vit K.

Good prospective study of doing nothing (Ann Emerg Med 40(1) 2002)

To read Leon Gussow’s 2005 Emergency Medicine News column on “Weapons of Mouse Destruction”, click here.

Share this:

  • Print
  • Email

Filed Under: 14. Toxicology


Creative Commons License 2012. This site represents the opinions of Crashing Patient LLC. See here for full disclaimer.

© 2023 ·