Organophosphate Toxicity Workup

  • Author: Kenneth D Katz, MD, FAAEM, ABMT; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM   more...
 
Updated: Jan 23, 2012
 

Laboratory Studies

Organophosphate (OP) toxicity is a clinical diagnosis. Confirmation of organophosphate poisoning is based on the measurement of cholinesterase activity; typically, these results are not readily available. Although RBC and plasma (pseudo) cholinesterase (PChE) levels can both be used, RBC cholinesterase correlates better with CNS acetylcholinesterase (AChE) and is, therefore, a more useful marker of organophosphate poisoning.

The portable Test-mate ChE field test measures RBC AChE and PChE within 4 minutes. A study of patients with acute organophosphorus poisoning compared Test-mate ChE results with those of a reference laboratory test and found good agreement between the two. Results show the Test-mate ChE field kit is a reliable test that provides rapid measurement of RBC AChE in acute organophosphorus poisoning.[11]

  • If possible, draw blood for measurement of RBC and plasma cholinesterase levels prior to treatment with pralidoxime (2-PAM). Monitoring serial levels can be used to determine a response to therapy.
  • RBC AChE represents the AChE found on RBC membranes, similar to that found in neuronal tissue. Therefore, measurement more accurately reflects nervous system OP AChE inhibition.
  • Plasma cholinesterase is a liver acute-phase protein that circulates in the blood plasma. It is found in CNS white matter, the pancreas, and the heart. It can be affected by many factors, including pregnancy, infection, and medical illness. Additionally, a patient's levels can vary up to 50% with repeated testing.
  • RBC cholinesterase is the more accurate of the 2 measurements, but plasma cholinesterase is easier to assay and is more readily available.

Cholinesterase levels do not always correlate with severity of clinical illness.

The level of cholinesterase activity is relative and is based on population estimates. Neonates and infants have baseline levels that are lower than adults. Because most patients do not know their baseline level, the diagnosis can be confirmed by observing a progressive increase in the cholinesterase value until the values plateau over time.

Falsely depressed levels of RBC cholinesterase can be found in pernicious anemia, hemoglobinopathies, use of antimalarial drugs, and oxalate blood tubes.

Falsely depressed levels of plasma cholinesterase are observed in liver dysfunction, low-protein conditions, neoplasia, hypersensitivity reactions, use of certain drugs (succinylcholine, codeine, morphine), pregnancy, and genetic deficiencies.

Other laboratory findings include: leukocytosis, hemoconcentration, metabolic and/or respiratory acidosis, hyperglycemia, hypokalemia, hypomagnesemia and elevated amylase and liver function studies A retrospective analysis of OP poisoned patients by Liu et al found a direct correlation between the severity of poisoning and mortality and the presence of pretreatment metabolic and respiratory acidosis.[12]

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Imaging Studies

A chest radiograph may reveal pulmonary edema but typically adds little to the clinical management of a poisoned patient.

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Other Tests

The true etiology of intermediate syndrome is still being investigated. Facts involved in its etiology as well as objective diagnostic tests may, in the near future, involve already available nerve testing techniques.[10] ECG findings include prolonged QTc interval, elevated ST segments, and inverted T waves. Although sinus tachycardia is the most common finding in the poisoned patient, sinus bradycardia with PR prolongation can develop with increasing toxicity due to excessive parasympathetic activation.

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Procedures

  • Endotracheal intubation and mechanical ventilation may be necessary in patients with organophosphate poisoning for airway protection and management of bronchorrhea and seizures.
  • Central venous access and arterial lines may be needed to treat the patient with organophosphate toxicity who requires multiple medications and blood-gas measurements.
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Contributor Information and Disclosures
Author

Kenneth D Katz, MD, FAAEM, ABMT  Assistant Professor, Division of Medical Toxicology, Department of Emergency Medicine, University of Pittsburgh Medical Center; Medical Director, Pittsburgh Poison Center

Kenneth D Katz, MD, FAAEM, ABMT is a member of the following medical societies: American Academy of Emergency Medicine and American College of Medical Toxicology

Disclosure: Nothing to disclose.

Coauthor(s)

Daniel E Brooks, MD  Co-Medical Director, Banner Good Samaritan Poison and Drug Information Center, Department of Medical Toxicology, Banner Good Samaritan Medical Center

Daniel E Brooks, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, and American College of Medical Toxicology

Disclosure: Nothing to disclose.

Specialty Editor Board

Lisa Kirkland, MD, FACP, CNSP, MSHA  Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; ANW Intensivists, Abbott Northwestern Hospital

Lisa Kirkland, MD, FACP, CNSP, MSHA is a member of the following medical societies: American College of Physicians, Society of Critical Care Medicine, and Society of Hospital Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Om Prakash Sharma, MD, FRCP, FCCP, DTM&H  Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California Keck School of Medicine

Om Prakash Sharma, MD, FRCP, FCCP, DTM&H is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Osler Society, American Thoracic Society, New York Academy of Medicine, and Royal Society of Medicine

Disclosure: Nothing to disclose.

Timothy D Rice, MD  Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, St Louis University School of Medicine

Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, FCCP, FCCM  Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease and Anesthesiology, Vice-Chair of Academic Affairs, Department of Critical Care Medicine, University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine

Michael R Pinsky, MD, CM, FCCP, FCCM is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Association of University Anesthetists, European Society of Intensive Care Medicine, Shock Society, and Society of Critical Care Medicine

Disclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights Board membership; Edwards Lifesciences Honoraria Consulting; Applied Physiology, Ltd Honoraria Consulting; Cheetah Medical Consulting fee Consulting

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Marina C Furtado, MD, and Lisa Chan, MD, FACEP, to the development and writing of this article.

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