insecticides, herbicides, rodenticides chapter 182 feb. 23, 2006
TRANSCRIPT
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Insecticides, Herbicides, Rodenticides
Chapter 182
Feb. 23, 2006
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Poisonings
• 2001 – 90,000 pesticide exposures reported
• Of these, 46, 929 were children under the age of 6
• There were 17 deaths
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Types of Exposure
• Three kinds…– Intentional– Accidental– Occupational
– Multiple formulations of the different compounds – always consult Poison Control
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Insecticides
• Toxic to nervous system– Four kinds
• Organophosphates• Carbamates• Organochlorines• Pyrethrins
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Organophosphates
• Diazinon, Malathion, Orthene, Parathion and chlorpyrifos have been used as chemical warfare agents since WWII
• Sarin, another compound used in the Tokyo subway in 1995
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Organophosphates
• Poisoning usually results in accidental exposure in the home, industrial accidents, agricultural sprayings, and in transport of these chemicals
• But also involved in intentional poisonings in homicides
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Organophosphates
• If patient presents with poisoning, clinician should ask about first-aid, prehospital interventions, decontamination, product name, manufacturer, product concentration and formulation, circumstances of exposure, amount , onset of symptoms and patient age and medical history
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Pathophysiology
• Inhibits the enzyme cholinesterase in the nervous system leading to an accumulation of the neurotransmitter acetylcholine in the CNS, the autonomic nervous system and at neuromuscular junctions.
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Pathophysiology
• This accumulation results in overstimulation of the receptors
• The initial overstimulation is followed by paralysis of cholinergic synaptic transmission in the CNS and autonomic ganglia
• A cholinergic crisis results
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Aging
• Aging describes the permanent irreversible binding of the compound to the cholinesterase
• Once aging occurs the enzymatic activity is permanently destroyed
• Can take weeks to synthesize new enzyme
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Clinical Features
• CNS symptoms of cholinergic excess include anxiety, restlessness, emotional lability, tremor, HA, dizziness, confusion, delirium, hallucinations and seizures
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Mnemonic Heaven
• S – Salivation• L – Lacrimation• U – Urination• D – Defecation• G – GI Pain• E - Emesis
• D – Defecation• U – Urination• M – Muscle wkness• B – BBB (Killer B’s)• E – Emesis• L – Lacrimation• S - Salivation
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Nicotinic Receptors
• Overstimulation results in pallor, mydriasis, tachycardia, HTN, muscle cramps and fasiculations, and then weakness and paralysis
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Special Considerations
• Children are at a greater risk of toxicity due to their size and lower baseline levels of cholinesterase activity
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Diagnosis
• Suspicion based on history
• Presence of a suggestive toxidrome
• Laboratory assays
• Testing for specific compounds
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Diagnosis
• Diagnosis can be difficult due to a constellation of clinical findings
• Misdiagnoses such as flu or viral syndrome have occurred
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Diagnosis
• Noting a hydrocarbon or garlic odor may help
• An initial test dose of atropine that does not result in expected improvement may help in making the diagnosis
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Diagnosis
• Unless 2-Pam (pralidoxime) is given before aging occurs, plasma cholinesterase takes up to 4-6 weeks and RBC acetylcholinesterase as long as 90-120 days to return to baseline
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Routine Labs
• Routine labs are non-diagnostic but may include evidence of pancreatitis, hypo or hyperglycemia, leukocytosis, and liver function abnormalities
• CXR may show pulmonary edema in severe cases
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EKG
• Common abnormalities include ventricular dysrhythmias, torsade de pointes, and idioventricular rhythms. Heart blocks and prolongation of QTC interval are common
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Treatment
• ABC’s
• Protective clothing must be worn to prevent contamination of health care workers (use neoprene or nitrile gloves instead of latex)
• Patient’s clothing must be removed and then disposed of in hazardous waste
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Treatment
• Patient must be washed in copious amounts of soap and water, with possible a second washing of dilute ethanol
• Body fluids are contaminated as well
• Runoff water must be contained and disposed of in hazardous materials
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Treatment
• Place patient on 100% O2, cardiac monitor and continuous pulse ox
• Suction airway as needed for bronchorrhea or emesis
• Coma, respiratory failure or seizures may necessitate intubation
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Treatment
• A nondepolarizing agent should be used for intubation, as Succinylcholine is metabolized by cholinesterase. Therefore prolonged paralysis may result
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Treatment
• Hypotension may need fluid boluses
• Charcoal is recommended for all ingestions
• Protect airway if you lavage, as lavage can be considered in recent or in large ingestions
• Hemodialysis has no proven value
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Treatment
• Atropine and pralidoxime are antidotes• Atropine is used to reverse muscarinic and
central effects• Large amounts may be needed – the dose
is titrated until copious bronchial secretions attentuate
• Pupillary dilatation is NOT the endpoint
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Atropine
• Atropine should not be withheld in the face of a tachycardia (heart rate may be the result of hypoxia)
• Initial test dose – 1 mg IV in adults, 0.01 to 0.04 mg/kg in children (but never less than 0.1mg)
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Atropine
• Normally that dose should produce antimuscarinic symptoms, but if no response to trial dose, then this is indicative of an organophosphate poisoning
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2-Pam
• Restores acetylcholinesterase activity by regenerating phosphorylated acetylcholinesterase
• Clinically, improves the muscarinic, nicotinic and CNS symptoms
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2-Pam
• Administer as soon as possible, though is still can be administered 24 to 48 hours after exposure
• Can reverse muscle paralysis if given soon enough before aging has occurred
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2-Pam
• Dose: 1-2 grams for adults and 20 to 40mg/kg – up to 1 gram in kids
• This is infused in NS over 5-10 minutes
• Can also be given IM
• A continuous infusion can be done (500 mg/hr in adults – 5-10 mg/kg/hr for kids) if paralysis does not resolve
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2-Pam
• Not administered to asymptomatic patients or to patients with known carbamate exposures presenting with minimal symptoms
• Response should occur within 10-40 minutes of administration
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Disposition
• Minimal exposure may just be decontamination and observation in ER for 6-8 hours
• Do not return clothing and discarded items to patient – DISCARD in hazardous waste
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Disposition
• For significant poisonings – ICU
• If toxins are fat soluble, then patient may be symptomatic for weeks
• Supportive care will be needed during this time, such as respiratory support
• End point of therapy is determined by absence of signs and symptoms
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Death
• Death usually occurs in 24 hours if patient is not treated
• Respiratory failure secondary to resp. muscle paralysis, CNS depression or bronchorrhea is usual cause of death
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Carbamates
• Sevin, Baygon, Lannate, Carbaryl, Aldicarb
• Cholinesterase inhibitors that are structurally related to organophosphates
• Medicinal forms include physostigmine, pyridostigmine and neostigmine
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Pathophysiology
• Transiently and reversibly inhibit cholinesterase
• Regeneration of enzyme occurs within minutes to hours, therefore aging does not occur
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Clinical Features
• Symptoms of intoxication are similar to organophosphates, but are of shorter duration
• Carbamates do not effective penetrate into CNS, so less central toxicity and no seizures
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Diagnosis
• Cholinesterase levels may return spontaneously to normal after 4-8 hours
• Measurement of cholinesterase activity generally is not useful as it will be relatively normal
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Treatment
• Atropine therapy usually not needed for longer than 6-12 hours
• Avoid 2-Pam. Since irreversible binding does not occur, it is not needed, and potentially can worsen some carbamate poisonings
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Organochlorines
• DDT is prototype
• Most have been restricted or banned in US due to their long half-life and toxicity
• Lindane is another common one used to treat head lice and scabies
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Pathophysiology
• CNS stimulant that can be toxic after dermal, inhalation and GI exposure
• Toxicity results from repetitive neuronal discharge following the action potential due to a decrease in the sodium channel permeability
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Pathophysiology
• Capable of inducing hepatic enzyme system, so the efficacy of other chemicals and drugs that use this system is reduced
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Clinical Features
• Neurologic symptoms predominate
• Mild poisonings present as dizziness, malaise, HA, irritability, delirium, myoclonus and facial paresthesias. Fever is common
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Clinical Features
• Severe poisonings may have seizures, coma, respiratory failure and death
• Seizures may occur early, have no prodromal syndromes and are short-lived
• Organochlorines are delivered dissolved in hydrocarbon solvents that can cause sedation, coma and pneumonitis
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Clinical Features
• Sensitization of the myocardium to endogenous cathecholamines with cardiac dysrythmias can occur from both the organochlorines and the solvents
• Chronic effects from low-level exposure to chlordane include deficits in balance, reaction times and verbal recall
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Diagnosis
• History is important!
• Read package label for the chemical involved and the vehicle involved
• Differential includes other causes of CNS stimulation and other insecticides
• Basic labs are not helpful but organochlorines can be detected in serum and urine by special laboratories
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Treatment
• O2, intubation if needed to treat hypoxia secondary to seizures, aspiration or resp. failure
• Benzos for seizure control
• Dysrhythmia control may be indicated but avoid atropine and epinephrine as the myocardium is sensitized to endogenous catecholamines
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Treatment
• Removal of clothing and washing skin with soap and water are important
• Avoid oils on skin as they promote absorption
• Charcoal and possibly gastric lavage in large recent ingestions are indicated
• Exchange resin Cholestyramine should be used in symptomatic Chlordecone exposures
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Disposition
• Observed for 6 hours and admitted to hospital if signs of significant toxicity develop or if ingestion involved a hydrocarbon solvent
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Pyrethrins
• Naturally occuring botanical substance found in chrysanthemum plants
• Used commonly as aerosols in insect sprays, so inhalation is most common exposure
• But also can be found in liquids and dusts in over the counter insecticides
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Pathophysiology
• Block the sodium channel at the neuronal cell membrane causing repetitive neuronal discharge
• Other effects include increased nicotinic cholinergie transmission, norepinephrine release and interference with sodium-calcium exchange
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Clinical Features
• Allergic hypersensitivity most common effect
• Manifest as dermatitis, asthma, rhinitis, pneumonitis and anaphylaxis
• Dermal absorption is minimal, but compounds are well-absorbed from GI tract
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Clinical Features
• Skin contact may lead to tingling and burning 30 minutes after exposure, but that dissipate within 24 hours
• Allergic reactions including fatal asthma attacks have been reported
• When absorbed, metabolized rapidly in liver, so minimal systemic toxicity
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Clinical Features
• Systemic symptoms would include paresthesia, hyperexcitablity, tremors, seizures, muscle weakness, respiratory failure, dizziness, HA and nausea.
• Vomiting and diarrhea seen in significant intentional ingestions
• Pulmonary edema, seizures, muscle fasciculations seen in severe poisonings
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Dx and Tx
• Differential includes allergic and neurologic diseases. Lab tests are of little value
• Treatment includes removal from exposure, dermal, ocular and gut decontamination, tx of allergic manifestations and supportive care. Hydrocarbon aspiration must be avoided
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Disposition
• Usually related to severity of exposure. Usually benign and hospitalization is not necessary
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DEET
• In OFF! and Skintastic
• In a variety of formulations ranging in concentrations of 5% to 100%
• Large margin of safety
• Absorbed through the skin
• Neurotoxin that causes seizures in large ingestions
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DEET
• Systemic toxicity manifests as restlessness, insomnia, altered behavior, confusion, CNS depression, slurred speech, ataxia, tremors, muscle cramps and hypertonia
• DEET induced hypotension and bradycardia have also been reported
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DEET
• Tx includes benzos for seizures, skin decontamination with soap and water, and activated charcoal for ingestions
• Most patients recover with supportive care
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Herbicides
• Chemicals used to kill weeds
• Formulations contain multiple ingredients such as solvents, surfactants and preservatives that may have their own toxic effects.
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Herbicides
• In 2001, there were 9378 exposures to herbicides
• Of these, 127 were intentional
• 2594 occurring in children younger than 6
• 4 deaths from Paraquat
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Chlorophenoxy Herb.
• Agent Orange was a mixture of two types (2,4-D and 2,4,5-T)
• These compounds are effective against broadleaf plants and also used as weed killers in lawns and grain crops
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Pathophysiology
• Metabolic pathway unknown
• Skeletal muscle toxicity can result in resp. failure or rhabdo
• Toxicity results from dermal contact, inhalation or ingestion
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Clinical Features
• After ingestion, N/V/D result
• Tachypnea may indicate pulmonary edema
• CV findings include hypotension, tachycardia and dysrhythmias
• Muscle toxicity findings include muscle tenderness, fasiculations, myotonia and rhabdo
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Clinical Features
• Patient may become hyperthermic
• Peripheral neuropathy has been described in the recovery phase and in chronic exposure
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Diagnosis
• Based on history• Ancillary tests nonspecific but may
demonstrate a metabolic acidosis and evidence of hepatorenal dysfunction
• Toxin levels not immediately available• Myoglobinuria and elevated CPK indicate
rhabdo• Differential includes other causes of
myopathy
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Treatment
• Supportive
• Decontamination measures and resp. support
• Alkalinization is suggested but not proven to increase the elimination of these compounds
• Treat the rhabdo
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Disposition
• Severe toxicity and serious complications are not common
• Since effects usually appear within 4-6 hours, patients with mild symptoms can be observed and discharged after that time
• Significant toxicity warrants admission
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Bipyridyl Herbicides
• Paraquat and diquat
• Ingestion responsible for most deaths
• Death has also been reported after transdermal exposure, ingestion and inhalation
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Pathophysiology
• Severe local irritant and devastating systemic toxin
• Ingested, it is absorbed rapidly
• Plasma concentrations peak within 2 hours of ingestion
• Distributed to most organs, with kidneys and lungs having the highest concentration
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Pathophysiology
• Acute exposure causes liver and renal necrosis, that is followed within a few weeks by pulmonary fibrosis
• Accumulated in the alveolar cells of the lungs, where it is transformed into a reactive oxygen species – a superoxide radical
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Pathophysiology
• Responsible for lipid peroxidation that leads to degradation of cell membranes, cell dysfunction and cell death
• Two phases – Initial destructive phase causes inflammatory cells and hemorrhage, but these changes may be reversible
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Pathophysiology
• Second proliferative phase involves fibrosis in the interstitium and alveolar spaces
• Myocardial injury and necrosis of the adrenals may occur
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Clinical Features
• Caustic effects produce local skin irritation and ulceration, as well as corneal injury in eye exposures
• Upper Resp Tract exposure may result in mucosal injury and epistaxis
• Inhalation may lead to cough, dyspnea, chest pain, pulmonary edema and hemoptysis
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Clinical Features
• Ingestion causes gastrointestinal mucosal lesions and ulcerations
• Hypovolemia occurs from GI fluid losses and decreased PO intake
• CV collapse may occur early in intoxication
• Seizures, GI perforation and hemorrhage and hepatic failure may occur
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Clinical Features
• Massive ingestions lead to multisystem failure and death within a few days
• Renal and hepatocellular necrosis develop b/w the 2nd and 5th days, with pulmonary fibrosis leading to hypoxemia 5 days to several weeks later
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Diagnosis
• History is important
• Qualitative and quantitative analyses for paraquat in urine and blood can assist you
• Nomograms used to predict survival based on plasma paraquat concentration and time of ingestion
• A 10 hour level greater than 0.4 mg/L carries a high probability of death
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Diagnosis
• Chemistry abnormalities may reflect multiorgan necrosis
• Hypokalemia may be present
• CXR show pneumonmediastinum or pneumothroax in the case of corrosive rupture of esophagus
• EGD should be performed to identify the extent of mucosal lesions
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Treatment
• Early and vigorous decontamination!
• Any exposure to paraquat is a medical emergency with hospitalization indicated even if patient is asymptomatic
• Attempt should be made to discourage superoxide radical formation by using low inspired oxygen to produce a hypoxemia to reduce pulmonary injury
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Treatment
• Using oxygen mixtures (FiO2 <21%) with positive pressure ventilation reduces pulm toxicity in experimental models and may be of therapeutic benefit
• Clothing removed and skin decontaminated with soap and water, but do not cause further abrasions that might increase systemic absorption
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Treatment
• Ocular irrigation with copious amounts of water or saline must take place
• Fluid and electrolyte losses need to be replaced
• Treat pain (from lesions) with opioids
• Emesis is common but gastric lavage via orogastric tube is recommended despite risk of perf.
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Treatment
• Gut decontamination is indicated as well
• Charcoal (1-2 g/kg), diatomaceous Fuller’s earth (1-2 g/kg in 15% aqueous suspension) or bentonite (1-2 g/kg in a 7% aqueous slurry)
• Repeat every 4 hours
• Sorbitol (70%) using 2ml/kg cathartic should be administered initially
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Treatment
• Charcoal hemoperfusion is known to remove paraquat and should be instituted as soon as possible and continued for 6-8 hours
• Support includes airway, maintaining intravascular volume, monitor vitals and ABG’s, pain relief, tx of renal failure and tx of infection
• MAINTAIN RENAL FUNCTION
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Disposition
• Attempt to determine prognosis
• Mortality rate from ingestion is as high as 75 %
• Recovery is usually without sequelae
• Ingestions of 20-40mg/kg usually results in death in 5 days to several weeks
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Disposition
• If more than a mouthful (50mg/kg) is ingested, death occurs within 72 hours
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Urea-Substituted Herb.
• Chlorimuron, diuron, fluometron, isopturon
• Low systemic toxicity
• Methemoglobinuria may occur
• Tx includes decontamination, supportive care and tx with methylene blue
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Organophosphorous Herb.
• Glyphosate (Roundup) is widely used
• Clinical effects include mucous membrane irritation and erosions, widespread organ dysfunction and refractory CV collapse
• Tx options are limited to charcoal and supportive care
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Rodenticides
• In 2001, there were 19,294 rodenticide exposures
• Long-acting superwarfarin agents accounted for 16,423 of these, most of which were in children less than 6 years of age
• 2 deaths, but none from the superwarfarins
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Rodenticides
• Nonanticoagulants– High toxicity
• Arsenic• Barium• Phosphorous• Strychine
– Moderate toxicity -Naphthylthiourea
– Low Toxicity• Red Squill• Norbormide• Bromethalin
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Rodenticides
• Anticoagulants– Warfarin types– Superwarfarins
– Single ingestions of Warfarin types are insignificant poisonings and do not usually cause bleeding problems
– Half-life of some superwarfarins are 120 days and can cause problems for weeks
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Clinical Approach
• Identifying product name is essential for management
• Specific odors or CNS, cardiopulmonary, GI, muscle or hemorrhagic manifestations may suggest a specific toxin
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Disposition
• Given the low frequency of physician experience with these types pf exposures, poison centers or toxicology consults must be used
• Threshold for hospital admission should be low
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Anticholinergic Toxicity
Chapter 183
Feb. 23, 2006
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Anticholinergics
• Should always be considered in patients that present to ED with unexplained mental status changes
• Antihistamine overdose is most common presentation
• In children, unintentional ingestion of just a few pills can result in significant toxicity
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Anticholinergics
• In elderly, therapeutic doses of certain pharmaceuticals may produce anticholinergic effects
• Intentional ingestions by teenagers is not uncommon – Alkaloid plants are abused for their hallucinogenic effects and group ingestions may result in multiple patients in your ED
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Pharmacologic Properties
• Anticholinergic refers to drugs and plant toxins that act as muscarinic receptor antagonists
• Drug absorption can occur after ingestion, smoking or ocular use
• Because these toxins slow GI motility, peak clinical effects are often delayed
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Anticholinergics
• Antihistamines
– Benadryl
– Dramamine
• AntiParkinsonian
– Cogentin
• Antipsychotics
– Thorazine
– Mellaril
– Clozapine
• Antispasmodics
– Bentyl
• Plants
– Deadly nightshade
– Jimsonweed
– Mandrake
• Skeletal Muscle Relaxants
– Norflex
– Flexeril
• Cyclic antidepressants
– Elavil
– Tofranil
– Sinequan
– Prozac
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Clinical presentations
• Mnemonic heaven…– Dry as a bone– Red as a beet– Hot as Hades– Blind as a bat– Mad as a hatter– Stuffed as a pipe
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Clinical Presentations
• Dry skin and dry mouth as a result of decreased sweat gland and salivary gland secretions
• Decreased bowel sounds as a result of decreased GI motility
• Palpable bladder secondary to urinary retention
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Clinical Presentations
• Tachycardia (120-160)
• Dilated pupils, though onset may be delayed 12-24 hours
• Delirium is common, with staccato speech pattern and difficult to comprehend speech
• Visual hallucinations, repetitive picking at bed clothes or imaginary objects have been observed
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Clinical Presentations
• Agitation-induced hyperthermia, esp when patient now has decreased sweating. This hyperthermia may result in multi-system organ dysfunction, resulting in liver, kidney and brain injury and coagulopathy.
• In some instances these changes are irreversible
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Clinical Presentations
• Central excitation and depression may both occur “agitated depression”
• Depressive features include lethargy, somnolence and coma
• Fatalities associated with overdose are characterized by severe agitation, status epilepticus, hyperthermia, wide-complex tachydysrhythmias and CV collapse
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Lab Evaluation
• Routine labs (incl. lytes, glucose and pulse ox) should be checked
• In most cases, these tests should be normal
• Limited UDS (drug screen) does not detect anticholinergics, though some pick up TCA’s
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Differential
• Viral Encephalitis
• Reye Syndrome
• Head Trauma
• ETOH withdrawl
• Postictal state
• Neuroleptic malignant syndrome
• Acute Psychiatric disorder
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Treatment
• Observation, monitoring and support
• Temperature monitoring essential
• GI decontamination may be warranted with charcoal, even after >1 hour post ingestion as decreased GI motility may still allow charcoal to help
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Treatment
• IV Bicarb to tx wide complex tachydysrhythmias
• Avoid class Ia agents as they have their own sodium channel blockade effect
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Treatment
• Major challenge is treating agitated patient
• Inadequate sedation may lead to worsening hyperthermia, rhabdo and injury
• Physical restraints may be needed, sedation is strongly recommended. Prolonged restraints may lead to further complications
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Treatment
• IV benzo’s such as lorazepam (2.5 mg IV) is appropriate first-line therapy
• Avoid phenothizines because of their anticholinergic effects
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Treatment
• Use of Physostigmine to reverse anticholinergic toxicity remains controversial
• Physostigmine is a reversible acetylcholinesterase inhibitor – crosses the blood-brain barrier
• This results in acetylcholine accumlation that reverses anticholinergic effects
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Treatment
• But may aggravate dysrhythmias and seizures and must be used with caution
• If used to treat drug overdoses that have sodium channel blockade (such as TCA’s) can cause bradycardia and asystole
• Patients without clear evidence of anticholinergic poisoning should not receive physostigmine
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Treatment
• Physostigmine can be considered in cases of severe agitation and delirium esp. in cases necessitation physical restraints for control no responsive to benzos
• Dose is 0.5 to 2.0 mg IV, slowly administered over 5 mintues
• When effective, a decrease in agitation may be seen in 15-20 minutes
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Treatment
• Because of rapid elimination, may need to repeat doses every 30-60 minutes
• Patients should be on a cardiac monitor and observed for signs of cholinergic excess (SLUDGE – remember?)
• Contraindications to physostigmine include asthma, cardiac conduction disturbances, suspected Na channel poisoning, or non-pharmacologically mediated intestinal or bladder obstruction
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Disposition
• Mild symptoms can be discharged after 6 hours of observation, if their symptoms have resolved
• More symptomatic patients require admission for at least 24 hours
• Because the half-life of physostigmine is shorter than the half-life of many anticholinergics, and the reversal effect may dissipate, resulting in recurrent toxicity, admission for continued observation is warranted in patients who received physostigmine