eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Organic Phosphorous Compounds and Carbamates: Treatment & Medication

Author: Daniel K Nishijima, MD, Staff Physician, Department of Emergency Medicine, University of California Davis Medical Center
Coauthor(s): Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center
Contributor Information and Disclosures

Updated: Sep 14, 2009

Treatment

Prehospital Care

Identification of the type of chemical is important in determining the patient's clinical course and prognosis. Emergency Medical Service (EMS) personnel should attempt to bring in the labels or the names of chemicals the patient was exposed to because different OPCs have different aging and reactivation times, which may help in guiding treatment. As a general rule, dimethyl OPCs undergo rapid aging, which makes early initiation of oximes critical. In comparison, diethyl compounds may cause delayed toxicity, and oxime therapy may need to be prolonged.14

Emergency Department Care

  • Airway, breathing, and circulation (ABCs): Care of the ABCs should be initiated first because intubation may be necessary in cases of severe poisoning. 
    • Because succinylcholine is metabolized by means of plasma cholinesterase, OPC or carbamate poisoning may cause prolonged paralysis. Increased doses of nondepolarizing agents, such as pancuronium or vecuronium, may be required to achieve paralysis because of the excess ACh at the receptor.10
    • Providers with appropriate personal protective equipment (PPE) can address the ABCs before decontamination.
  • Decontamination: Decontamination is an important part of the initial care. In general, the importance of decontamination depends on the route of poisoning. Patients with dermal and inhalation exposures, as expected in a terrorist attack, are more likely to cause nosocomial poisoning than patients with GI exposure. Patients with GI exposure should also be decontaminated, but ED staff should not delay urgent treatment with excessive decontamination, given that nosocomial poisoning from GI exposure is rare and controversial. Patients with dermal and inhalation poisonings must be decontaminated before being brought into the ED if it was not done in the prehospital setting.
    • Case reports have described nosocomial poisoning in staff members treating patients who have been exposed to OPCs and carbamates4,15,16 ; one describes OPC toxicity from mouth-to-mouth resuscitation17 . Only one case discusses serious poisoning in which a staff member required treatment and eventual intubation.18 However, none of these cases was confirmed with diagnostic studies.
    • In addition, nosocomial OPC poisoning has not been reported in developing countries with a high incidence of severe OPC poisoning.
    • Moreover, the odors often smelled when one cares for a patient poisoned from pesticide are commonly due to the hydrocarbon solvent, which may cause symptoms independent of the OPC agent.19
    • The patient's clothes must be removed and isolated, and his or her body washed with soap and water.
  • GI decontamination
    • Oral administration of activated charcoal is a reasonable intervention after GI poisoning. However, as with any poisoned patient, the risks and benefits must be weighed.
    • While a recent systematic review20 did not find any clear evidence supporting gastric lavage, the authors recommend it in patients who present early after ingestion and have no vomiting and in patients who require intubation due to acute ingestion of an OPC or carbamate.
  • Atropine: Atropine is a pure muscarinic antagonist that competes with ACh at the muscarinic receptor.
    • Atropine is most commonly given in intravenous (IV) form at the recommended dose of 2-5 mg for adults and 0.05 mg/kg for kids with a minimum dose of 0.1 mg to prevent reflex bradycardia. Atropine may be redosed every 5-10 minutes. Severe OP poisonings often require hundreds of milligrams of atropine.
    • In one case report, a patient required frequent doses of atropine and was eventually converted to an atropine infusion to a total of 30 g over 5 days.21
    • Most sources recommend starting atropine on patients with anything more than ocular effects and then observing the drying of secretions as an endpoint in titrating to the appropriate dose.
    • From the Tokyo sarin experience, patients poisoned by nerve agents had modest atropine requirements, with none requiring more than 10 mg.
  • Oximes: The only oxime available in the United States is pralidoxime (2-PAM).
    • OPCs and carbamates bind and phosphorylate one of the active sites of AChE and inhibit the functionality of this enzyme. Oximes bind to the OP or carbamate, causing the compound to break its bond with AChE. Most of the effects are on the peripheral nervous system because entry into the CNS is limited.
    • Atropine does not bind to nicotinic receptors; therefore, it is ineffective in treating neuromuscular toxicity (particularly weakness of respiratory muscles).
    • The main therapeutic effect of pralidoxime is predicted to be recovery of neuromuscular transmission at nicotinic synapses. However, oximes also enhance cholinesterase activity at muscarinic sites, decreasing the requirement for atropine. In vitro experiments have shown that oximes are effective reactivators of human AChE inhibited by OP compounds.22
    • In some situations, reactivation of inhibited AChE by oximes is likely to be absent or limited when affinity for the particular OP-AChE complex is poor, the dose or duration of treatment is insufficient, the OP persists in the patient and therefore rapid reinhibition of the newly reactivated enzyme occurs, and the inhibited AChE ages.
    • The degree of reactivation depends on the specific identities and concentrations of the oxime and the OP.23,24,25,22 Because diethyl-OP–inhibited AChEs reactivate and age notably slower than the dimethyl analogs, they generally require prolonged oxime treatment.26 The half-lives of aging of dimethyl phosphorylated or diethyl phosphorylated AChE, as determined in isolated human RBCs in vitro, are 3.7 or 33 hours, respectively, and the therapeutic windows (4 times the half-life) are a maximum of 13 or 132 hours, respectively.27,28
    • Although animal data28 and observational clinical data25,27,29 suggest regeneration of AChE and improved outcome, only a few randomized controlled studies have been done.
      • One study by Johnson et al was a comparison of pralidoxime 1 g as a bolus, with pralidoxime 12 g as an infusion (no bolus) over 4 days. Mortality rates, need for ventilation, and rates of intermediate syndrome were higher with the infusion group than with the bolus group.30
      • Another study by Cherian et al was a comparison of pralidoxime 12 g given over 3 days with placebo. Results were similar in both groups, with increased rates of mortality, ventilatory support, and intermediate syndrome.31
      • A more recent randomized study by Pawar et al in patients with moderately severe anticholinesterase pesticide poisoning (all patients received initial 2 g bolus dosing of pralidoxime over 30 min) compared continuous pralidoxime infusion of 1 g/h versus pralidoxime 1 g every 4 hours. Patients with the continuous pralidoxime infusion were found to have decreased atropine requirements and decreased need for intubation.32
    • Both the 1-g bolus dose and the 12-g infusion dose fall short of WHO-recommended dosing for adults, which is a bolus of at least 30 mg/kg followed by an infusion of at least 8 mg/kg/h. Pediatric dosing is a 25-50 mg/kg bolus given over 30 minutes then an infusion of 10-20 mg/kg/h. This WHO recommendation is based on the doses known to achieve serum pralidoxime concentration of greater than 4 mg/L, the minimum effective concentration reported in an early study.33 Randomized controlled studies with oxime therapy at the WHO-recommended doses are needed to further delineate its effectiveness.
    • The WHO protocol for oxime therapy is recommended for any patient with clinically significant poisoning.
  • Benzodiazepines: Seizures are an uncommon complication of OP poisoning. When they occur, they represent severe toxicity. As with most seizures of toxicologic etiology, benzodiazepines are the preferred medication.
  • Other treatments: Prospective studies of both magnesium and fresh-frozen plasma as adjunctive therapy in OP poisoning have shown improved mortality rates with both treatments.34,35 However, both must be evaluated further. Nebulized ipratropium bromide may also have therapeutic effects as an adjunct agent.

Consultations

Consult a regional poison control center or toxicologist for further recommendations for patient care. Consult a psychiatrist in any intentional or suspected intentional ingestions.

Medication

Control of clinically significant cholinergic excess is the key to management. Anticholinergic agents can be used to substantially reduce or eliminate the secretory effects of muscarinic excess. Endpoints for therapy include elimination of bronchorrhea (atropine) and improved muscle strength (oximes). Reaching these endpoints may require more medication than commonly prescribed.

GI decontaminant

This drug is used to bind recently ingested agents, thereby limiting systemic absorption. It is not useful for noningestion exposures.


Activated charcoal (Liqui-Char)

Reduces systemic absorption through the alimentary tract. Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present adsorbs 100-1000 mg of drug per gram charcoal. Does not dissolve in water. For maximum effect, administer within 30 min of poison ingestion.

Adult

1 g/kg PO; first dose usually with cathartic, though not necessary if diarrhea, due to cholinergic stimulation is present; not to exceed 50-100 g; may repeat 0.5 g/kg q4h (alternate use of cathartic; monitor for active bowel sounds)

Pediatric

<2 years: 1-2 g/kg PO; up to 15-30 g; may repeat 0.5 g/kg q4h (alternate use of cathartic, if using, and monitor for active bowel sounds)
>2 years: Administer as in adults

May inactivate ipecac syrup if used concomitantly; decreases effectiveness of coadministered medications; do not mix with sherbet, milk, or ice cream (decreases adsorptive properties)

Documented hypersensitivity; poisoning or overdose of mineral acids and alkalies; unprotected airway with absent gag reflex

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for active bowel sounds before readministration to minimize risk of charcoal ileus; not effective in ethanol, methanol, or iron-salt poisoning; induce emesis before administration; after emesis with ipecac syrup, patient may not tolerate activated charcoal for 1-2 h; can administer in early stages of gastric lavage; without sorbitol, gastric lavage returns are black

Antidotes

Anticholinergics, such as atropine, cause pharmacologic antagonism of excess anticholinesterase activity at muscarinic receptors. Oximes reverse the inhibition of AChE and nicotinic effects, including muscle paralysis.


Atropine (Atropair)

Used for GI or pulmonary distress in known or suspected OP or carbamate poisonings. Continue until bronchoconstriction and bronchorrhea controlled. High doses may be required in first 24 h of treatment. Treatment may be required for 48 h in severe cases. May need to reduce doses with concurrent oximes.

Adult

Initial or diagnostic: 1 mg IV
Therapeutic: 2-4 mg IV q15min until pulmonary secretions dry;
prolonged 2 mg/kg/h IV infusion might be needed to control secretions

Pediatric

Initial or diagnostic: 0.015 mg/kg IV
Therapeutic: 0.015-0.05 mg/kg IV q15min until secretions substantially reduced

Additive effects with coadministered anticholinergics; pharmacologic effects of atenolol and digoxin may increase; antipsychotic effects of phenothiazines may decrease; tricyclic antidepressants with anticholinergic activity may increase effects

Documented hypersensitivity; thyrotoxicosis; narrow-angle glaucoma; tachycardia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in Down syndrome and/or brain damage to prevent hyperreactive response; caution in coronary heart disease, congestive heart failure, cardiac arrhythmias, and hypertension; caution in peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy, prostatism can cause dysuria, and catheterization may be needed


Pralidoxime (2-PAM, Protopam)

Indications include muscle weakness (especially respiratory) in known or suspected OP poisoning. Rarely needed in carbamate poisonings. Muscle strength should increase in 30 min. Must be used early in poisoning, before OP-AChE bond has aged, to be effective. May help prevent intermediate and delayed neuromuscular and neuropsychiatric OP syndromes.

Adult

At least 30 mg/kg IV over 15 min initially; then 8 mg/kg/h IV until muscle strength improves

Pediatric

25-50 mg/kg IV over 30 min initially; then 10-20 mg/kg/h IV until muscle strength improves

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Relatively nontoxic compounds; not effective for OP poisonings caused by without anticholinesterase activity

Benzodiazepine

This drug is used to control seizures.


Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing GABA activity.

Adult

5-10 mg IV over 3-5 min

Pediatric

30 days to 5 years: 0.2-0.5 mg IV slowly q2-5min until symptoms resolve; not to exceed 5 mg
>5 years: 1 mg IV slowly q2-5min until symptoms resolve; not to exceed 10 mg

Effects potentiated by phenothiazines, narcotics, barbiturates, MAOIs, and other antidepressants

Documented hypersensitivity; acute narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity); monitor for respiratory depression with high or repeated doses


Lorazepam (Ativan)

DOC for treatment of status epilepticus because persists in CNS longer than diazepam. Rate of injection not to exceed 2 mg/min. May be administered IM if IV access not available.

Adult

0.044 mg/kg (range, 2-4 mg) IV, titrate to effect
Status epilepticus: 4 mg IV over 2-5 min; may repeat in 10-15 min if needed; not to exceed 8 mg

Pediatric

Children: 0.05 mg/kg IV (range, 0.02-0.1 mg/kg)
Adolescents: Administer as in adults
Status epilepticus:
Neonates: 0.05 mg/kg IV over 2-5 min; may repeat in 10-15 min if needed
Infants and children: 0.1 mg/kg IV over 2-5 min; not to exceed 4 mg; second dose 0.05 mg/kg IV at 10-15 min, if needed
Adolescents: 0.7 mg/kg IV slowly over 2-5 min; not to exceed 4 mg; may repeat in 10-15 min, if needed

Alcohol, phenothiazines, barbiturates, and MAOIs increase CNS toxicity

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Monitor for respiratory depression with high or repeated doses; contains benzyl alcohol, which may be toxic to infants in high doses; caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, Parkinson disease, or inhibited benzodiazepine metabolism and clearance (eg, in use of nicotine or cimetidine)


Midazolam (Versed)

Alternative to terminate refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Wait 2-3 min to fully evaluate sedative effects before starting procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if vascular access unavailable.

Adult

0.01-0.05 mg/kg IV slowly over several min; usually 0.5-4 mg, not to exceed 10 mg; may repeat q10-15min until adequate response achieved

Pediatric

<32 weeks: 0.5 mcg/kg/min IV infusion
>32 weeks: 1 mcg/kg/min IV infusion
Children: 0.05-0.2 mg/kg IV over 2-3 min, followed by 1-2 mcg/kg/min continuous infusion
Status epilepticus (refractory to standard therapy), >2 months and children: 0.15 mg/kg then continuous infusion 1 mcg/kg/min; titrate upward q5min until seizures controlled

Theophyllines may antagonize sedative effects; narcotics, cimetidine, ethanol, and erythromycin may accentuate sedative effects because of decreased clearance; reduce dose of thiopental by 15% when used together

Documented hypersensitivity; preexisting hypotension; narrow-angle glaucoma; sensitivity to propylene glycol (diluent)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, pulmonary disease, renal impairment, hepatic failure, neuromuscular disease, hypotension, and patients >60 y; monitor for respiratory depression with high or repeated doses; consider reduced doses in organic brain syndrome and inhibited benzodiazepine metabolism and clearance (eg, in use of nicotine or cimetidine)

More on Toxicity, Organic Phosphorous Compounds and Carbamates

Overview: Toxicity, Organic Phosphorous Compounds and Carbamates
Differential Diagnoses & Workup: Toxicity, Organic Phosphorous Compounds and Carbamates
Treatment & Medication: Toxicity, Organic Phosphorous Compounds and Carbamates
Follow-up: Toxicity, Organic Phosphorous Compounds and Carbamates
References
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Further Reading

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Keywords

pesticide exposure, organic phosphorous compound poisoning, OPC poisoning, carbamate poisoning, pesticide poisoning, pesticides, physostigmine, neostigmine, nerve agent, self-poisoning, toxic ingestion, toxidrome, suicidal ingestion, accidental ingestion, Tokyo subway sarin attack, VX, soman, agricultural exposure, organophosphate toxicity, carbamate toxicity, organophosphate exposure, carbamate exposure, pesticide toxicity

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Contributor Information and Disclosures

Author

Daniel K Nishijima, MD, Staff Physician, Department of Emergency Medicine, University of California Davis Medical Center
Daniel K Nishijima, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center
Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Dana A Stearns, MD, Assistant Director of Undergraduate Education, Department of Emergency Medicine, Massachusetts General Hospital
Dana A Stearns, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Fred Harchelroad, MD, FACMT, FAAEM, FACEP, Chair, Department of Emergency Medicine, Director of Medical Toxicology - Allegheny General Hospital, Associate Professor, Department of Emergency Medicine, Drexel University College of Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

 
 
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