CBRNE - Nerve Agents, G-series - Tabun, Sarin, Soman Workup

Updated: Oct 02, 2021
  • Author: Kermit D Huebner, MD, FACEP; Chief Editor: Duane C Caneva, MD, MSc  more...
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Approach Considerations

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 red blood cell (RBC) cholinesterase.

Respiratory impairment in nerve agent intoxication produces expected derangement in arterial blood gas values, including a reduction in partial pressure of arterial oxygen (PaO2).

Hypokalemia has been reported in GB intoxication, although the mechanism is unclear.

Chest x-ray may be helpful in treating patients with significant pulmonary symptoms.

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 electroencephalographic monitoring is recommended for patients paralyzed from nerve agent exposure, because paralysis from nicotinic effects of these agents may mask seizures from CNS effects.


Red Blood Cell Cholinesterase

RBC cholinesterase and plasma cholinesterase (pseudocholinesterase) appear to have a physiologic role as buffers for the tissue acetylcholinesterases found in the nervous system. These two 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.