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Pralidoxime (Systemic)


VA CLASSIFICATION
Primary: AD900

Commonly used brand name(s): Protopam Chloride.

Other commonly used names are:
2-PAM {04} {12} {16} {26} and 2-PAM chloride . {01} {04} {10} {13} {19}
Note: For a listing of dosage forms and brand names by country availability, see Dosage Forms section(s).



Category:


Antidote (to organophosphate pesticides)—

antidote (to organophosphate chemicals)—

antidote (to cholinesterase inhibitors)—

Indications

Accepted

Toxicity, organophosphate pesticide (treatment adjunct)
Toxicity, organophosphate chemical (treatment adjunct) or
Toxicity, cholinesterase inhibitor (treatment adjunct)—Pralidoxime is indicated as an adjunct in the treatment of moderate and severe {09} poisoning caused by organophosphate pesticides that have anticholinesterase activity or by chemicals with anticholinesterase activity such as some chemicals used as nerve agents during chemical warfare. {01} {02} {05} {09} {10} {11} {14} {31} Pralidoxime is also indicated as an adjunct in the management of overdose of cholinesterase inhibitors, such as ambenonium, neostigmine, and pyridostigmine, used in the treatment of myasthenia gravis. {01} {02}
—Pralidoxime, used in conjunction with atropine, reverses nicotinic effects, such as muscle weakness and fasciculation, respiratory depression, {01} {06} {12} {14} {17} {26} and central nervous system (CNS) effects, {12} {14} {26} {34} associated with toxic exposure to organophosphate anticholinesterase pesticides and chemicals and with cholinesterase inhibitor overdose. {23} {24} {25} Atropine, by antagonizing the action of cholinesterase inhibitors at muscarinic receptor sites, reverses muscarinic effects, such as tracheobronchial and salivary secretion, bronchoconstriction, bradycardia, {06} {09} {14} {15} {17} and, to a moderate extent, CNS effects. {06} {16} Atropine does not reverse nicotinic effects. {08} {14} {15}
—Pralidoxime should also be used in poisonings in which the patient presents with symptoms typical of acetylcholinesterase inhibition, although the source of the poisoning is not known, or in which the patient suffers from mixed organophosphate-carbamate pesticide poisoning. {05} {18} {28} {34} {35}

Acceptance not established
Use of pralidoxime in the treatment of carbamate pesticide poisoning is controversial {33} {34} (except in carbaryl poisoning, in which the use of pralidoxime is not recommended). {01} {06} {09} {28} {31} {32} In a manner similar to that of organophosphates, carbamates inhibit acetylcholinesterase; but unlike the bond formed between organophosphates and cholinesterase, the carbamate-cholinesterase bond is reversible and readily dissociates. {05} {33} {34} {35} The effects of the poisoning are short-lived and usually can be resolved with atropine and supportive care. {05} {28} Pralidoxime has been used in a small number of patients to treat the nicotinic effects of carbamate poisoning. {33} {34} {35} However, more experience is needed to determine that resolution of nicotinic effects of carbamate poisoning is actually potentiated by administration of pralidoxime, and not merely due to spontaneous recovery of acetylcholinesterase activity. {36}

Unaccepted
Pralidoxime should not be used in the treatment of poisoning caused by the carbamate pesticide, carbaryl. {01} {06} {09} {28} {31} {32} Pralidoxime has been shown in animal studies to enhance the severity of the poisoning. {09} {15} {16} {28} {30} {31} {32}

Pralidoxime is not effective in the treatment of poisoning caused by phosphorus, inorganic phosphates, or organophosphates not having anticholinesterase activity. {01} {10}


Pharmacology/Pharmacokinetics

Physicochemical characteristics:
Molecular weight—
    172.61 {04}


pH
    Auto-injection: 2 to 3. {10}
    Reconstituted solution: 3.5 to 4.5. {01} {02} {03}

Mechanism of action/Effect:

Antidote to organophosphate pesticides and chemicals and to cholinesterase inhibitors—Organophosphates bind to the esteratic site of acetylcholinesterase, resulting initially in reversible inactivation of the enzyme. {14} If given within 24 hours, and possibly up to 48 hours, after organophosphate exposure, pralidoxime reactivates the enzyme {01} {05} {06} {07} {08} {09} {10} {11} {13} {14} {17} {20} {26} by cleaving the phosphate-ester bond formed between the organophosphate and acetylcholinesterase. {05} {07} {14} {20} After 24 to 48 hours, the bond “ages” and acetylcholinesterase cannot be reactivated by pralidoxime. {01} {02} {09} {14} {16} {20} Pralidoxime also slows the process of aging of phosphorylated acetylcholinesterase to a nonreactivatable form and detoxifies certain organophosphates by direct chemical action. {01} {05} {10}

Note: In high doses, pralidoxime may inhibit acetylcholinesterase {06} and cause neuromuscular blockade. {06} {09}


Distribution:

Distributed throughout the extracellular water. {01} {10}

Protein binding:

Not bound to plasma proteins. {01} {10} {13}

Biotransformation:

Metabolized largely by the liver. {06}

Half-life:

Elimination—Approximately 1.2 hours. {01} {09} {10} {11} {17} {29}

Onset of action:

Within 10 to 40 minutes. {01} {09} {10} {11} {12}

Minimum therapeutic concentration:

4 mcg per mL {01} {10} {13} {17} (23.17 micromoles per L).

Elimination:
    Rapidly excreted in the urine, {01} {06} {10} {13} {17} {29} partly unchanged, and partly as a metabolite produced by the liver. {01} {10}


Precautions to Consider

Carcinogenicity/Mutagenicity

Studies have not been done to evaluate the carcinogenic or mutagenic potential of pralidoxime. {01} {10}

Pregnancy/Reproduction

Pregnancy—
Studies have not been done in humans.

Studies have not been done in animals.

FDA Pregnancy Category C. {01}

Breast-feeding

It is not known whether pralidoxime is distributed into breast milk.

Pediatrics

Appropriate studies on the relationship of age to the effects of pralidoxime have not been performed in the pediatric population. However, pediatrics-specific problems that would limit the usefulness of this medication in children are not expected. {02} {05} {09} {11} {12} {14} {16} {18}


Geriatrics


Appropriate studies on the relationship of age to the effects of pralidoxime have not been performed in the geriatric population. However, no geriatrics-specific problems have been documented to date.

Drug interactions and/or related problems
The following drug interactions and/or related problems have been selected on the basis of their potential clinical significance (possible mechanism in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):


Note: Combinations containing any of the following medications, depending on the amount present, may also interact with this medication.

Barbiturates{01}{10}    (poisoning with organophosphates sensitizes the medullary centers to depression by barbiturates {02})


CNS depression–producing medications{01}{02}{05}{10}{16} (See Appendix II ) or
Xanthines,{01}{02}{05}{10}{16}{18} such as:
» Aminophylline
» Caffeine
» Theophylline    (use of these medications may exacerbate the effects of organophosphate poisoning)


» Succinylcholine{01}{02}{10}{33}    (succinylcholine is metabolized by plasma cholinesterases, which are inhibited in organophosphate poisoning or cholinesterase inhibitor overdose; therefore, prolonged respiratory paralysis could occur {11} {12})


Thiamine{17}{29}    (concurrent administration of intravenous thiamine may delay initial excretion of pralidoxime, probably by competing at a common renal excretory site)



Laboratory value alterations
The following have been selected on the basis of their potential clinical significance (possible effect in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

With physiology/laboratory test values
Alanine aminotransferase (ALT [SGPT]) and
Aspartate aminotransferase (AST [SGOT]) and
Creatine kinase (CK)    (transient increases in values have been seen in healthy volunteers; values returned to normal within approximately 2 weeks {01} {10})


Medical considerations/Contraindications
The medical considerations/contraindications included have been selected on the basis of their potential clinical significance (reasons given in parentheses where appropriate)— not necessarily inclusive (» = major clinical significance).


Risk-benefit should be considered when the following medical problems exist
» Myasthenia gravis{01}    (pralidoxime should be used with caution to avoid precipitating a myasthenic crisis)


» Renal function impairment{01}{02}{10}    (pralidoxime is excreted via the kidneys; reduction in dose is recommended)


Sensitivity to pralidoxime{01}{10}

Patient monitoring
The following may be especially important in patient monitoring (other tests may be warranted in some patients, depending on condition; » = major clinical significance):


Note: Initiation of therapy must not be delayed until the results of the tests recommended below are available. {01} {05} {10} {11} {16} {18} However, blood should be drawn prior to initiation of pralidoxime therapy to establish baseline red blood cell acetylcholinesterase and pseudocholinesterase concentrations. {16} {21} {35} Pralidoxime causes these concentrations to lose their diagnostic significance. {12} {16} {35}

Acetylcholinesterase, red blood cell (RBC)    (a measure of true cholinesterase activity that correlates with the concentration of acetylcholine present at receptor sites; {12} {15} recommended prior to administration of pralidoxime {16} to confirm diagnosis of organophosphate poisoning; {01} {05} {06} {08} {09} {10} {15} {16} {18} {21} a history of exposure to organophosphates and a reduction in acetylcholinesterase concentration below 50% of normal laboratory or pre-exposure values are consistent with poisoning {01} {10} {16})


Electrocardiogram (ECG)    (recommended to detect arrhythmias, {02} especially in patients with pulmonary edema {05} or patients who are severely poisoned {07} or unconscious {05})


Paranitrophenol, urinary    (recommended to confirm diagnosis and monitor clinical progress of parathion toxicity {01} {10})


Pseudocholinesterase, serum    (a measure of cholinesterase found in the liver and serum; {05} {09} recommended to assess the degree of exposure to organophosphate pesticides or chemicals {05} {07} {09} and to monitor clinical progress; {01} {10} {11} {20} {21} pseudocholinesterase concentrations may be decreased in patients with liver disease, {05} {07} {21} malnutrition, {05} {07} {21} acute infections, {05} anemias, {05} myocardial infarction, {05} dermatomyositis, {05} {07} and a genetically determined enzyme deficiency, as well as in patients with organophosphate poisoning; {05} {07} {09} {12} {15} low concentrations may also be seen in patients taking estrogens or oral contraceptives {21})




Side/Adverse Effects

Note: Many of the following side/adverse effects have been reported only in normal volunteers given pralidoxime, not in patients given pralidoxime after exposure to organophosphate pesticides or chemicals. {01} {10}
In patients treated for poisoning it is difficult to differentiate the side/adverse effects produced by atropine or the organophosphate pesticides or chemicals from those produced by pralidoxime. {01} {07} {10}

The following side/adverse effects have been selected on the basis of their potential clinical significance (possible signs and symptoms in parentheses where appropriate)—not necessarily inclusive:

Those indicating need for medical attention
Incidence more frequent
    
Blurred{01}{06}{09}{10}{14}{16}{29} or double{01}{02}{09}{10}{14}{16}{19} vision
    
dizziness {01}{02}{07}{09}{10}{14}{16}{19}
    
hyperventilation (rapid breathing){01}{10}{19}
    
impaired accommodation (difficulty in focusing eyes){01}{02}{10}{14}
    
increased blood pressure {01}{10}{16}{19}
    
laryngospasm (difficulty in speaking or breathing){01}{14}{27}
    
muscle rigidity{01}{14} or weakness{01}{10}{19}
    
pain at injection site —following intramuscular administration{01}{10}
    
tachycardia (fast heartbeat){01}{09}{14}{16}{19}

Note: Increased blood pressure, {39} laryngospasm, muscle rigidity, and tachycardia may be caused by a too-rapid rate of intravenous administration. {01} {09} {14} {16} {19} These effects may be avoided by keeping the rate of injection at less than 500 mg per minute. {02} {06} {09}




Those indicating need for medical attention only if they continue or are bothersome
Incidence more frequent
    
Drowsiness {01}{10}{19}
    
headache {01}{02}{09}{10}{14}{16}{19}
    
nausea {01}{07}{09}{10}{14}{16}{19}





Patient Consultation
As an aid to patient consultation, refer to Advice for the Patient, Pralidoxime (Systemic).

In providing consultation, consider emphasizing the following selected information (» = major clinical significance):

Before using this medication
»   Conditions affecting use, especially:
Sensitivity to pralidoxime
Other medications, especially xanthines, such as aminophylline, caffeine, and theophylline
Other medical problems, especially myasthenia gravis or renal function impairment

Proper use of this medication

For auto-injector dosage form
Receiving training and reading patient instructions carefully before need to use medication

Importance of not removing safety cap before ready to use

Procedures for using auto-injector

Removing gray safety cap

Placing black tip of device on thigh with injector pointed at thigh

Pressing hard into thigh until auto-injector functions; holding in place several seconds; removing and discarding as directed

Massaging injected area for 10 seconds

» Importance of not using more medication than the amount recommended

For all dosage forms

» Proper dosing

» Proper storage

Precautions while using this medication
Avoiding use of CNS depressants


Side/adverse effects
Signs of potential side effects, especially blurred or double vision, dizziness, hyperventilation, impaired accommodation, increased blood pressure, laryngospasm, muscle rigidity or weakness, pain at injection site, and tachycardia


General Dosing Information
For more information on the management of organophosphate pesticide or chemical toxicity, or cholinesterase inhibitor overdose, contact a poison control center (see Poison Control Center Listing ).

For treatment of organophosphate pesticide or chemical toxicity
Initial treatment of organophosphate pesticide or chemical toxicity should be directed toward decontamination {09} and maintenance or restoration of adequate ventilation. {05} Removing nasopharyngeal secretions {01} {02} {06} {07} {09} {10} and administering oxygen {06} {08} {16} or otherwise assisting respiration are essential. Provision of an artificial airway may also be necessary. {02} {06} {10} {11} {15} {16} It is important that those attending to the patient protect themselves from contamination. {02} {07} {09} {11} {12} {18} If the patient has had dermal exposure, the clothing should be removed {08} and the hair, skin, {06} {09} {10} {16} and fingernails {38} washed thoroughly, first with sodium bicarbonate, then with alcohol. {01} {02} {10} {11} Soap and water {02} may be used if sodium bicarbonate and alcohol are not available. If there has been ocular involvement, the eyes should be flushed with a gentle stream of water {02} {09} for at least 15 minutes. {09} {11}

If the organophosphate has been inhaled, exposure should be terminated by removing the patient from the environment {06} {08} {09} and, if the air remains contaminated, administering oxygen. {06} {08}

Ingested organophosphates should be removed by gastric lavage with protection of the airway, if necessary. Gastric lavage is most effective when instituted within 30 minutes after ingestion because organophosphates are rapidly absorbed from the gastrointestinal tract. {09} {16} {18} Activated charcoal should be administered {37} to reduce further absorption. Induced emesis with ipecac syrup should be avoided because unconsciousness may develop before emesis occurs. {09}

Once adequate ventilation has been established, atropine should be administered intravenously. For adults, the dose is 2 to 4 mg, repeated every 5 to 10 minutes; for children, the dose is 0.05 to 0.1 mg per kg of body weight administered on a similar schedule. {01} {36} In severe poisoning, a more aggressive escalation of the dose may be needed. {40} Administration of atropine should be continued until signs of atropine toxicity (delirium; {01} {02} {06} {22} dilated pupils; {16} {18} {22} dry mouth; {16} {18} {22} muscle twitching; {01} {02} {06} tachycardia—if bradycardia was an earlier sign; {16} {18} {22} warm, dry, and flushed skin {08} {16} {18} {22}) appear or until secretions are inhibited. {08} {22} Atropine should not be given in the presence of hypoxia because of the risk of inducing ventricular fibrillation. {01} {02} {09} {10} {11} Some degree of atropinization should be maintained for at least 48 hours. {01} {02} {06} {07}

Pralidoxime should be administered after the effects of atropine become apparent. However, pralidoxime becomes ineffective as an antidote when administered more than 24 to 48 hours postexposure as a result of aging of the phosphate-ester bond. {01} {02} {09} {14} {16} {20} The preferred route of administration of pralidoxime is intravenous. However, pralidoxime may be administered intramuscularly {01} {10} {11} or subcutaneously {01} if intravenous administration is not possible. Treatment with atropine and pralidoxime should continue until there is symptomatic improvement and restoration of acetylcholinesterase activity, as determined by measurement of red blood cell acetylcholinesterase. {09} The patient should be monitored closely for 48 to 72 hours. {01} {02} {07} {10}

Many of the alkyl phosphates are extremely lipid soluble, and if extensive partitioning into body fat has occurred, the onset of symptoms may be delayed and may recur after initial treatment. In some cases it has been necessary to continue treatment with atropine and pralidoxime for several weeks. {06}

Diazepam may be given to relieve anxiety {09} {11} or to control seizures not responsive to atropine. {01} {06} {08} {09} {10} {11} {18}

For treatment of cholinesterase inhibitor toxicity
Cholinesterase inhibitor toxicity, or cholinergic crisis, must be distinguished from myasthenic crisis, either on the basis of presenting signs and symptoms or through the use of edrophonium. {23} {24} {25}

To control the increased gastrointestinal stimulation and muscarinic effects associated with cholinergic crisis, atropine may be administered intravenously at an initial dose of 2 to 4 mg followed by 2 mg every 5 to 10 minutes until muscarinic effects disappear or signs of atropine toxicity appear. {22} Pralidoxime may then be administered to treat the nicotinic effects. {23}


Parenteral Dosage Forms

PRALIDOXIME CHLORIDE USP

Note: The pralidoxime chloride auto-injector is specifically designed for use by military personnel or qualified civilian emergency responders. {10}


Usual adult dose
Toxicity, organophosphate chemical
Intramuscular, 600 mg. The dose may be repeated two times at fifteen-minute intervals, if necessary. {10}


Usual pediatric dose
Dosage has not been established.

Usual geriatric dose
See Usual adult dose .

Strength(s) usually available
U.S.—


600 mg per 2 mL (Rx)[Generic](benzyl alcohol 20 mg per mL)(aminoacetic acid 11.26 mg per mL)(water for injection){10}

Note: Pralidoxime auto-injectors are available through the Directorate of Medical Material of the Defense Personnel Support Center or other analogous local, state, or federal agencies. {10}


Canada—
Not commercially available.

Packaging and storage:
Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F), unless otherwise specified by manufacturer. Protect from freezing. {10}


PRALIDOXIME CHLORIDE STERILE USP

Usual adult and adolescent dose
Toxicity, organophosphate pesticide
Intravenous: 1 to 2 grams {01} {02} {05} {06} {07} {09} {11} {12} {18} {19} injected at a rate not to exceed 500 mg per minute {02} {09} {18} or infused over fifteen to thirty minutes. {01} {02} {05} {12} The dose may be repeated after one hour, {01} {02} {06} {09} {12} {16} {18} and then at eight- to twelve-hour intervals {09} {11} {14} if muscle weakness persists.

Toxicity, cholinesterase inhibitor
Intravenous, initially, 1 to 2 grams followed by 250 mg every five minutes. {01}


Note: Reduction in dose is recommended in the presence of renal function impairment. {01} {02}


Usual adult prescribing limits
Twelve grams within twenty-four hours. {09}

Usual pediatric dose
Toxicity, organophosphate pesticide
Intravenous infusion: 25 to 50 mg per kg of body weight {02} {05} {09} {11} {12} {14} {16} {18} over fifteen to thirty minutes. {05} {09} {11} {12} {14} {16} The dose may be repeated after one hour, {01} {02} {06} {09} {12} {16} {18} and then at eight- to twelve-hour intervals {09} {11} {14} if muscle weakness persists.

Toxicity, cholinesterase inhibitor
Dosage has not been established.


Usual geriatric dose
See Usual adult and adolescent dose .

Size(s) usually available:
U.S.—


1 gram (Rx) [Protopam Chloride]{01}

Canada—


1 gram (Rx) [Protopam Chloride]{02}

Packaging and storage:
Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F), unless otherwise specified by manufacturer.

Preparation of dosage form:
For intravenous injection, 20 mL of sterile water for injection should be added to each 1-gram vial. {01} {02}

For intravenous infusion, the solution should be prepared as described for preparation of injection. This solution may be further diluted with 0.9% sodium chloride injection {01} {12} to a final concentration of 1 to 2%. {01}

Stability:
Pralidoxime should be used promptly after reconstitution and any remaining solution discarded. {01}



Revised: 04/01/1996



References
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Further information

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