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Neostigmine consists of a carbamate moiety and a quaternary ammonium group (Figure 12–4). The former provides covalent bonding to acetylcholines-terase. The latter renders the molecule lipid insoluble, so that it cannot pass through the blood–brain barrier.
The maximum recommended dose of neostigmine is 0.08 mg/kg (up to 5 mg in adults), but smaller
amounts often suffice and larger doses have also been given safely ( Table 12–3). Neostigmine is most commonly packaged as 10 mL of a 1 mg/mL solu-tion, although 0.5 mg/mL and 0.25 mg/mL concen-trations are also available.
The effects of neostigmine (0.04 mg/kg) are usually apparent in 5min, peak at 10 min, and last more than 1 hr. If reversal is not complete in 10 min after 0.08 mg/kg, the time for full recovery of neuromus-cular function will depend on the nondepolarizing agent used and the intensity of blockade. In practice, many clinicians use a dose of 0.04 mg/kg (or 2.5 mg) if the preexisting blockade is mild to moderate and a dose of 0.08 mg/kg (or 5 mg) if intense paralysis is being reversed. The duration of action is prolonged in geriatric patients. Muscarinic side effects are minimized by prior or concomitant administration of an anticholinergic agent. The onset of action of glycopyrrolate (0.2 mg glycopyrrolate per 1 mg of neostigmine) is similar to that of neostigmine and is associated with less tachycardia than is experi-enced with atropine (0.4 mg of atropine per 1 mg of neostigmine). It has been reported that neostigmine crosses the placenta, resulting in fetal bradycardia. Thus, theoretically, atropine may be a better choice of an anticholinergic agent than glycopyrrolate in pregnant patients receiving neostigmine, but there is no evidence that this makes any difference in patient outcomes. Neostigmine is also used to treat myas-thenia gravis, urinary bladder atony, and paralytic ileus.
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