Edrophonium test

Edrophonium test. An intravenous injection of edrophonium chloride which is a drug that blocks the degradation of acetylcholine and temporarily increases the levels of acetylcholine at the neuromuscular junction. 

Edrophonium is sometimes used as a diagnostic test for myasthenia. A 2 mg dose is injected intravenously after baseline muscle strength has been measured. If no reaction occurs after 45 seconds, an additional 8 mg may be injected. If the patient has myasthenia gravis, an improvement in muscle strength that lasts about 5 minutes can usually be observed. 

Edrophonium is available in multiple-dose or singledose 10-mg/ml ampules. An accessible vein is foimd on one of the patient s arms, and a butterfly infusion set with a 27-gauge needle is attached to a 1-ml tuberculin syringe containing 10 mg edrophonium solution. Initially, 2 mg (0.2 ml) edrophonium is injected intravenously. A saline flush may follow this injection to confirm appropriate dose administration. If after 1 or 2 minutes definite improvement in ptosis or ocular misalignment occurs, the test is considered positive and no further edrophonium injection is necessary. If no definite improvement occurs, however, another 3 mg (0.3 ml) edrophonium is injected and the patient is again observed. 

The neostigmine test is used more often to help evaluate limb strength in suspected myasthenics. Neostigmine, a reversible cholinesterase inhibitor with a duration of action longer than that of edrophonium, can be administered either intravenously or intramuscularly. The usual adult dose is 1.5 mg intramuscularly in combination with 0.5 mg atropine to prevent cholinergic-induced side effects. 

Excessive dosing with an anticholinesterase can actually worsen the muscle weakness in myasthenics if the accumulation of acetylcholine at the neuromuscular junction is sufficient to cause depolarising blockade cholinergic crisis). It is important to distinguish this type of muscle weakness from an exacerbation of the disease itself myasthenic crisis). The dilemma can be resolved with a test dose of edrophonium, which relieves a myasthenic crisis but worsens a cholinergic one. The latter may be severe enough to precipitate respiratory failure and should be attempted only with full resuscitation facilities, including mechanical ventilation, at hand. 

Cerebrospinal flnid is normal in botnlism bnt nsnally abnormal with other causes of neurologic illnesses. Brain, spine, and chest imaging may reveal other causes of the neurologic symptoms, such as hemorrhage, inflammation or neoplasm (36). Myasthenia gravis patients with paralysis will obtain brief relief from a test dose of edrophonium chloride, whereas a close inspection of the skin may reveal the cause of tick paralysis (36). 

This is a nonpharmacologic test that can be performed to assess for MG. This is a positive finding, but it does not apply to edrophonium. 

A library of novel AChE reactivators based on imidazole aldoximes and N-substituted 2-hydroxyiminoacet-amides (35-36 Figure 72.28) was screened by Sit et al. (2011). Compounds were screened for reactivation of sarin-, cyclosarin-, VX-, and paraoxon-inhibited human AChE. Reactivators exhibited reactivation activity that was comparable or greater than that of pralidoxime, monoisonitrosoacetone (MINA), and 2,3-butanedione monooxime. Unfortunately, standard substances used in this field (i.e., obidoxime and asoxime) were not compared in this study. More recently, some oximes from this library were tested against tabun-inhibited human AChE (Kovarik et al., 2013). Some selected compounds were able to reactivate tabim inhibition with a performance comparable to pralidoxime, but they were not as effective as the bisquatemary standards trimedoxime and obidoxime. Radic et al. (2012) published presented pyridinium and non-pyridinium oxime reactivators derived from pralidoxime and edrophonium (37-39 Figure 72.29). Compounds were tested on cyclosarin-, VX-, and paraoxon-inhibited human AChE and BChE and compared to pralidoxime and asoxime. Some novel compounds were found to be better reactivators than... 

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