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Insecticides, Herbicides, Rodenticides. Chapter 182 Feb. 23, 2006. Poisonings. 2001 – 90,000 pesticide exposures reported Of these, 46, 929 were children under the age of 6 There were 17 deaths. Types of Exposure. Three kinds… Intentional Accidental Occupational

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poisonings
Poisonings
  • 2001 – 90,000 pesticide exposures reported
  • Of these, 46, 929 were children under the age of 6
  • There were 17 deaths
types of exposure
Types of Exposure
  • Three kinds…
    • Intentional
    • Accidental
    • Occupational
    • Multiple formulations of the different compounds – always consult Poison Control
insecticides
Insecticides
  • Toxic to nervous system
    • Four kinds
      • Organophosphates
      • Carbamates
      • Organochlorines
      • Pyrethrins
organophosphates
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
organophosphates6
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
organophosphates7
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
pathophysiology
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.
pathophysiology9
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
aging
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
clinical features
Clinical Features
  • CNS symptoms of cholinergic excess include anxiety, restlessness, emotional lability, tremor, HA, dizziness, confusion, delirium, hallucinations and seizures
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

Mnemonic Heaven
nicotinic receptors
Nicotinic Receptors
  • Overstimulation results in pallor, mydriasis, tachycardia, HTN, muscle cramps and fasiculations, and then weakness and paralysis
special considerations
Special Considerations
  • Children are at a greater risk of toxicity due to their size and lower baseline levels of cholinesterase activity
diagnosis
Diagnosis
  • Suspicion based on history
  • Presence of a suggestive toxidrome
  • Laboratory assays
  • Testing for specific compounds
diagnosis16
Diagnosis
  • Diagnosis can be difficult due to a constellation of clinical findings
  • Misdiagnoses such as flu or viral syndrome have occurred
diagnosis17
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
diagnosis18
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
routine labs
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
slide20
EKG
  • Common abnormalities include ventricular dysrhythmias, torsade de pointes, and idioventricular rhythms. Heart blocks and prolongation of QTC interval are common
treatment
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
treatment22
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
treatment23
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
treatment24
Treatment
  • A nondepolarizing agent should be used for intubation, as Succinylcholine is metabolized by cholinesterase. Therefore prolonged paralysis may result
treatment25
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
treatment26
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
atropine
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)
atropine28
Atropine
  • Normally that dose should produce antimuscarinic symptoms, but if no response to trial dose, then this is indicative of an organophosphate poisoning
2 pam
2-Pam
  • Restores acetylcholinesterase activity by regenerating phosphorylated acetylcholinesterase
  • Clinically, improves the muscarinic, nicotinic and CNS symptoms
2 pam30
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
2 pam31
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
2 pam32
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
disposition
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
disposition34
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
death
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
carbamates
Carbamates
  • Sevin, Baygon, Lannate, Carbaryl, Aldicarb
  • Cholinesterase inhibitors that are structurally related to organophosphates
  • Medicinal forms include physostigmine, pyridostigmine and neostigmine
pathophysiology37
Pathophysiology
  • Transiently and reversibly inhibit cholinesterase
  • Regeneration of enzyme occurs within minutes to hours, therefore aging does not occur
clinical features38
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
diagnosis39
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
treatment40
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
organochlorines
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
pathophysiology42
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
pathophysiology43
Pathophysiology
  • Capable of inducing hepatic enzyme system, so the efficacy of other chemicals and drugs that use this system is reduced
clinical features44
Clinical Features
  • Neurologic symptoms predominate
  • Mild poisonings present as dizziness, malaise, HA, irritability, delirium, myoclonus and facial paresthesias. Fever is common
clinical features45
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
clinical features46
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
diagnosis47
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
treatment48
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
treatment49
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
disposition50
Disposition
  • Observed for 6 hours and admitted to hospital if signs of significant toxicity develop or if ingestion involved a hydrocarbon solvent
pyrethrins
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
pathophysiology52
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
clinical features53
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
clinical features54
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
clinical features55
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
dx and tx
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
disposition57
Disposition
  • Usually related to severity of exposure. Usually benign and hospitalization is not necessary
slide58
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
slide59
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
slide60
DEET
  • Tx includes benzos for seizures, skin decontamination with soap and water, and activated charcoal for ingestions
  • Most patients recover with supportive care
herbicides
Herbicides
  • Chemicals used to kill weeds
  • Formulations contain multiple ingredients such as solvents, surfactants and preservatives that may have their own toxic effects.
herbicides62
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
chlorophenoxy herb
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
pathophysiology64
Pathophysiology
  • Metabolic pathway unknown
  • Skeletal muscle toxicity can result in resp. failure or rhabdo
  • Toxicity results from dermal contact, inhalation or ingestion
clinical features65
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
clinical features66
Clinical Features
  • Patient may become hyperthermic
  • Peripheral neuropathy has been described in the recovery phase and in chronic exposure
diagnosis67
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
treatment68
Treatment
  • Supportive
  • Decontamination measures and resp. support
  • Alkalinization is suggested but not proven to increase the elimination of these compounds
  • Treat the rhabdo
disposition69
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
bipyridyl herbicides
Bipyridyl Herbicides
  • Paraquat and diquat
  • Ingestion responsible for most deaths
  • Death has also been reported after transdermal exposure, ingestion and inhalation
pathophysiology71
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
pathophysiology72
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
pathophysiology73
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
pathophysiology74
Pathophysiology
  • Second proliferative phase involves fibrosis in the interstitium and alveolar spaces
  • Myocardial injury and necrosis of the adrenals may occur
clinical features75
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
clinical features76
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
clinical features77
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
diagnosis78
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
diagnosis79
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
treatment80
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
treatment81
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
treatment82
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.
treatment83
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
treatment84
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
disposition85
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
disposition86
Disposition
  • If more than a mouthful (50mg/kg) is ingested, death occurs within 72 hours
urea substituted herb
Urea-Substituted Herb.
  • Chlorimuron, diuron, fluometron, isopturon
  • Low systemic toxicity
  • Methemoglobinuria may occur
  • Tx includes decontamination, supportive care and tx with methylene blue
organophosphorous herb
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
rodenticides
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
rodenticides90
Nonanticoagulants

High toxicity

Arsenic

Barium

Phosphorous

Strychine

Moderate toxicity

-Naphthylthiourea

Low Toxicity

Red Squill

Norbormide

Bromethalin

Rodenticides
rodenticides91
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
clinical approach
Clinical Approach
  • Identifying product name is essential for management
  • Specific odors or CNS, cardiopulmonary, GI, muscle or hemorrhagic manifestations may suggest a specific toxin
disposition93
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
anticholinergic toxicity

Anticholinergic Toxicity

Chapter 183

Feb. 23, 2006

anticholinergics
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
anticholinergics96
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
pharmacologic properties
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
anticholinergics98
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

Anticholinergics
clinical presentations
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
clinical presentations100
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
clinical presentations101
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
clinical presentations102
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
clinical presentations103
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
lab evaluation
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
differential
Differential
  • Viral Encephalitis
  • Reye Syndrome
  • Head Trauma
  • ETOH withdrawl
  • Postictal state
  • Neuroleptic malignant syndrome
  • Acute Psychiatric disorder
treatment106
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
treatment107
Treatment
  • IV Bicarb to tx wide complex tachydysrhythmias
  • Avoid class Ia agents as they have their own sodium channel blockade effect
treatment108
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
treatment109
Treatment
  • IV benzo’s such as lorazepam (2.5 mg IV) is appropriate first-line therapy
  • Avoid phenothizines because of their anticholinergic effects
treatment110
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
treatment111
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
treatment112
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
treatment113
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
disposition114
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
ad