Laboratory Studies
In the acute care setting, laboratory studies should include glucose, BUN, electrolytes, prothrombin time, liver function studies, and cholinesterase measurements.
Levels of plasma and/or RBC cholinesterase enzyme may be measured by any of several existing methods. Most frequently used, because it is most readily available, is the test for plasma (or pseudo) cholinesterase (PChE). Because this can be affected by other disorders, it does not confirm the diagnosis. Mild intoxication is diagnosed when RBC cholinesterase inhibition is less than 50% of normal. Depression of this value by 25% or more is confirmatory; this test may be used to follow progress. Workers exposed to organophosphates used in agriculture should have a baseline level recorded.
The Test-mate ChE 400 is a portable field kit used to detect occupational organophosphorus exposure. The test measures RBC AChE and plasma cholinesterase (PChE) within 4 minutes. A study of patients with acute organophosphorus self-poisoning compared Test-mate ChE results to reference laboratory tests and found good agreement between the two. The Test-mate ChE kit provides rapid and reliable measurement of RBC AChE levels. [16]
Imaging Studies
The only imaging study that may be useful in acute management is a chest radiograph because of the danger of aspiration pneumonia in a confused patient with vomiting and compromised respiration.
Other Tests
See the list below:
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Electrocardiography should be done on admission, since many patients develop cardiac irregularities following acute exposure.
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Electrophysiologic studies
Acute organophosphate toxicity producing weakness is due to sustained endplate depolarization. In vivo microelectrode studies reported by Maselli and Soliven demonstrated no reduction in the amplitude of miniature endplate potentials or of the quantal content of the endplate potentials. Repetitive stimulation produced a decremental response as the endplate was "flooded" with acetylcholine. [17]
Rutchik and Rutkove found a temperature-dependent response; cooling to 32°C produced a normal-amplitude compound action potential (CMAP). A smaller spontaneous repetitive response was elicited in a man with organophosphate intoxication. Warming the limb to 39°C caused these responses to decrease in amplitude; the authors likened the effect to that seen in myasthenia gravis. [18]
De Luca et al have described a technique for evaluating neuromuscular involvement by measuring changes in the firing pattern of surface electromyography. Studies in rhesus monkeys showed gaps in the motor unit recruitment following a dose of OP. This pattern may reflect the tremor related to the degree of OP exposure. [19]
Singh et al examined the phrenic nerve conduction of 29 patients with organophosphate toxicity admitted to the hospital in 1997, 14 of whom required mechanical ventilation. They found that reduction in CMAP correlated with need for ventilatory assistance. By following patients with daily studies, they were able to predict successful weaning. [20]
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Neuropsychological testing: Workers exposed over a long period to pesticides have been reported to manifest irritability, fatigue, headache, and difficulties with memory and concentration.
Histologic Findings
Nerve biopsy in late-onset neuropathy reveals a primary axonopathy with secondary demyelination. CNS myelin may be lost as well.
