Insecticides, Herbicides, Rodenticides

1
Insecticides, Herbicides, Rodenticides

• Chapter 182
• Feb. 23, 2006

2
Poisonings

• 2001 90,000 pesticide exposures reported
• Of these, 46, 929 were children under the age of
  6
• There were 17 deaths

3
Types of Exposure

• Three kinds
• Intentional
• Accidental
• Occupational
• Multiple formulations of the different compounds
  always consult Poison Control

4
Insecticides

• Toxic to nervous system
• Four kinds
• Organophosphates
• Carbamates
• Organochlorines
• Pyrethrins

5
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

6
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

7
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

8
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.

9
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

10
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

11
Clinical Features

• CNS symptoms of cholinergic excess include
  anxiety, restlessness, emotional lability,
  tremor, HA, dizziness, confusion, delirium,
  hallucinations and seizures

12
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 Bs)
• E Emesis
• L Lacrimation
• S - Salivation

13
Nicotinic Receptors

• Overstimulation results in pallor, mydriasis,
  tachycardia, HTN, muscle cramps and
  fasiculations, and then weakness and paralysis

14
Special Considerations

• Children are at a greater risk of toxicity due to
  their size and lower baseline levels of
  cholinesterase activity

15
Diagnosis

• Suspicion based on history
• Presence of a suggestive toxidrome
• Laboratory assays
• Testing for specific compounds

16
Diagnosis

• Diagnosis can be difficult due to a constellation
  of clinical findings
• Misdiagnoses such as flu or viral syndrome have
  occurred

17
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

18
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

19
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

20
EKG

• Common abnormalities include ventricular
  dysrhythmias, torsade de pointes, and
  idioventricular rhythms. Heart blocks and
  prolongation of QTC interval are common

21
Treatment

• ABCs
• Protective clothing must be worn to prevent
  contamination of health care workers (use
  neoprene or nitrile gloves instead of latex)
• Patients clothing must be removed and then
  disposed of in hazardous waste

22
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

23
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

24
Treatment

• A nondepolarizing agent should be used for
  intubation, as Succinylcholine is metabolized by
  cholinesterase. Therefore prolonged paralysis
  may result

25
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

26
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

27
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)

28
Atropine

• Normally that dose should produce antimuscarinic
  symptoms, but if no response to trial dose, then
  this is indicative of an organophosphate poisoning

29
2-Pam

• Restores acetylcholinesterase activity by
  regenerating phosphorylated acetylcholinesterase
• Clinically, improves the muscarinic, nicotinic
  and CNS symptoms

30
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

31
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

32
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

33
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

34
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

35
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

36
Carbamates

• Sevin, Baygon, Lannate, Carbaryl, Aldicarb
• Cholinesterase inhibitors that are structurally
  related to organophosphates
• Medicinal forms include physostigmine,
  pyridostigmine and neostigmine

37
Pathophysiology

• Transiently and reversibly inhibit cholinesterase
• Regeneration of enzyme occurs within minutes to
  hours, therefore aging does not occur

38
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

39
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

40
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

41
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

42
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

43
Pathophysiology

• Capable of inducing hepatic enzyme system, so the
  efficacy of other chemicals and drugs that use
  this system is reduced

44
Clinical Features

• Neurologic symptoms predominate
• Mild poisonings present as dizziness, malaise,
  HA, irritability, delirium, myoclonus and facial
  paresthesias. Fever is common

45
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

46
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

47
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

48
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

49
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

50
Disposition

• Observed for 6 hours and admitted to hospital if
  signs of significant toxicity develop or if
  ingestion involved a hydrocarbon solvent

51
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

52
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

53
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

54
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

55
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

56
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

57
Disposition

• Usually related to severity of exposure. Usually
  benign and hospitalization is not necessary

58
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

59
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

60
DEET

• Tx includes benzos for seizures, skin
  decontamination with soap and water, and
  activated charcoal for ingestions
• Most patients recover with supportive care

61
Herbicides

• Chemicals used to kill weeds
• Formulations contain multiple ingredients such as
  solvents, surfactants and preservatives that may
  have their own toxic effects.

62
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

63
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

64
Pathophysiology

• Metabolic pathway unknown
• Skeletal muscle toxicity can result in resp.
  failure or rhabdo
• Toxicity results from dermal contact, inhalation
  or ingestion

65
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

66
Clinical Features

• Patient may become hyperthermic
• Peripheral neuropathy has been described in the
  recovery phase and in chronic exposure

67
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

68
Treatment

• Supportive
• Decontamination measures and resp. support
• Alkalinization is suggested but not proven to
  increase the elimination of these compounds
• Treat the rhabdo

69
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

70
Bipyridyl Herbicides

• Paraquat and diquat
• Ingestion responsible for most deaths
• Death has also been reported after transdermal
  exposure, ingestion and inhalation

71
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

72
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

73
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

74
Pathophysiology

• Second proliferative phase involves fibrosis in
  the interstitium and alveolar spaces
• Myocardial injury and necrosis of the adrenals
  may occur

75
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

76
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

77
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

78
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

79
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

80
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

81
Treatment

• Using oxygen mixtures (FiO2 lt21) 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

82
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.

83
Treatment

• Gut decontamination is indicated as well
• Charcoal (1-2 g/kg), diatomaceous Fullers 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

84
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 ABGs,
  pain relief, tx of renal failure and tx of
  infection
• MAINTAIN RENAL FUNCTION

85
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

86
Disposition

• If more than a mouthful (50mg/kg) is ingested,
  death occurs within 72 hours

87
Urea-Substituted Herb.

• Chlorimuron, diuron, fluometron, isopturon
• Low systemic toxicity
• Methemoglobinuria may occur
• Tx includes decontamination, supportive care and
  tx with methylene blue

88
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

89
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

90
Rodenticides

• Nonanticoagulants
• High toxicity
• Arsenic
• Barium
• Phosphorous
• Strychine
• Moderate toxicity
• ?-Naphthylthiourea

• Low Toxicity
• Red Squill
• Norbormide
• Bromethalin

91
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

92
Clinical Approach

• Identifying product name is essential for
  management
• Specific odors or CNS, cardiopulmonary, GI,
  muscle or hemorrhagic manifestations may suggest
  a specific toxin

93
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

94
Anticholinergic Toxicity

• Chapter 183
• Feb. 23, 2006

95
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

96
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

97
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

98
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

99
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

100
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

101
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

102
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

103
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

104
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 TCAs

105
Differential

• Viral Encephalitis
• Reye Syndrome
• Head Trauma
• ETOH withdrawl
• Postictal state
• Neuroleptic malignant syndrome
• Acute Psychiatric disorder

106
Treatment

• Observation, monitoring and support
• Temperature monitoring essential
• GI decontamination may be warranted with
  charcoal, even after gt1 hour post ingestion as
  decreased GI motility may still allow charcoal to
  help

107
Treatment

• IV Bicarb to tx wide complex tachydysrhythmias
• Avoid class Ia agents as they have their own
  sodium channel blockade effect

108
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

109
Treatment

• IV benzos such as lorazepam (2.5 mg IV) is
  appropriate first-line therapy
• Avoid phenothizines because of their
  anticholinergic effects

110
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

111
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 TCAs) can cause
  bradycardia and asystole
• Patients without clear evidence of
  anticholinergic poisoning should not receive
  physostigmine

112
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

113
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

114
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