CBRNE - Nerve Agents, G-series - Tabun, Sarin, Soman Workup
- Author: Kermit D Huebner, MD, FACEP; Chief Editor: Robert G Darling, MD, FACEP more...
Laboratory Studies
Although no laboratory test exists to directly measure nerve agent levels in serum or urine, the acute effects of nerve agents can be estimated by measuring the percent reduction in the activity of erythrocytic (RBC) cholinesterase.
RBC cholinesterase and plasma cholinesterase (pseudocholinesterase) appear to have a physiologic role as buffers for the tissue AChEs found in the nervous system. These 2 enzymes are clinically important, because their activities can be assayed directly in blood, whereas the tissue cholinesterases cannot. Activity of RBC cholinesterase is considered a more sensitive indicator of nerve agent toxicity than that of plasma cholinesterase.
Despite the clinical use of RBC cholinesterase, keep certain limitations in mind when using the activity of RBC cholinesterase to interpret nerve agent effects. Activity of RBC cholinesterase is subject to some individual variation. Without establishing the baseline value of RBC cholinesterase in individuals, measuring the percent reduction in enzyme activity is difficult.
Poor correlation exists between clinical effects of nerve agents and the percent reduction of RBC cholinesterase activity at low-dose exposures. Accordingly, RBC cholinesterase activity always must be correlated with the patient's clinical status and never should determine patient disposition alone.
A good guideline is that severe clinical effects tend to correlate with a 20-25% reduction in RBC cholinesterase activity. A rising RBC cholinesterase level indicates that no further nerve agent absorption is occurring and that the enzyme is regenerating. RBC cholinesterase is replaced fully every 120 days at the natural regeneration rate of RBCs (approximately 1%/d). Draw blood for RBC cholinesterase activity level prior to administering oxime antidotes.
Respiratory impairment in nerve agent intoxication produces expected derangement in arterial blood gas values, including a reduction in PaO2.
Hypokalemia has been reported in GB intoxication, although the mechanism is unclear.
Imaging Studies
- Chest x-ray may be helpful in treating patients with significant pulmonary symptoms.
Other Tests
- A number of electrocardiographic changes have been reported in nerve agent intoxication, including bradycardia and varying degrees of atrioventricular block (first through third degree) from the direct muscarinic effect on the heart and tachycardia and ventricular dysrhythmias from hypoxia. Nerve agent toxicity has been associated with PR interval prolongation, QT prolongation, and torsade de pointes.
- Bedside EEG monitoring is recommended for patients paralyzed from nerve agent exposure, because paralysis from nicotinic effects of these agents may mask seizures from CNS effects.
Holstege CP, Kirk M, Sidell FR. Chemical warfare. Nerve agent poisoning. Crit Care Clin. Oct 1997;13(4):923-42. [Medline].
Sidell FR. Nerve agents. In: Medical Aspects of Chemical and Biological Warfare. 1987:129-179.
Kato T, Hamanaka T. Ocular signs and symptoms caused by exposure to sarin gas. Am J Ophthalmol. Feb 1996;121(2):209-10. [Medline].
Nozaki H, Hori S, Shinozawa Y, et al. Relationship between pupil size and acetylcholinesterase activity in patients exposed to sarin vapor. Intensive Care Med. Sep 1997;23(9):1005-7. [Medline].
Rickett DL, Glenn JF, Beers ET. Central respiratory effects versus neuromuscular actions of nerve agents. Neurotoxicology. Spring 1986;7(1):225-36. [Medline].
Nakajima T, Sato S, Morita H, Yanagisawa N. Sarin poisoning of a rescue team in the Matsumoto sarin incident in Japan. Occup Environ Med. Oct 1997;54(10):697-701. [Medline].
Okumura T, Takasu N, Ishimatsu S, et al. Report on 640 victims of the Tokyo subway sarin attack. Ann Emerg Med. Aug 1996;28(2):129-35. [Medline].
Sidell FR, Borak J. Chemical warfare agents: II. Nerve agents. Ann Emerg Med. Jul 1992;21(7):865-71. [Medline].
Tokuda Y, Kikuchi M, Takahashi O. Prehospital management of sarin nerve gas terrorism in urban settings: 10 years of progress after the Tokyo subway sarin attack. Resuscitation. Feb 2006;68(2):193-202. [Medline].
National Center for Disaster Preparedness. Atropine Use in Children After Nerve Gas Exposure. Pediatric Expert Advisory Panel (PEAP) Info Brief. Spring 2004;1:[Full Text].
McDonough JH. Midazolam: An Improved Anticonvulsant Treatment for Nerve Agent Induced Seizures. Defense Technical Information Center. JAN 2002;[Full Text].
Dunn MA, Hackley BE, Sidell FR. Pretreatment for nerve agent exposure. In: Medical Aspects of Chemical and Biological Warfare. 1987:181-196.
Yokoyama K, Araki S, Murata K, et al. A preliminary study on delayed vestibulo-cerebellar effects of Tokyo Subway Sarin Poisoning in relation to gender difference: frequency analysis of postural sway. J Occup Environ Med. Jan 1998;40(1):17-21. [Medline].
Nakajima T, Ohta S, Fukushima Y, Yanagisawa N. Sequelae of sarin toxicity at one and three years after exposure in Matsumoto, Japan. J Epidemiol. Nov 1999;9(5):337-43. [Medline].
Chao LL, Rothlind JC, Cardenas VA, Meyerhoff DJ, Weiner MW. Effects of low-level exposure to sarin and cyclosarin during the 1991 Gulf War on brain function and brain structure in US veterans. Neurotoxicology. Sep 2010;31(5):493-501. [Medline]. [Full Text].
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