The decision is made to proceed to the operating room for emergency evacuation of subdural hematoma. Rapid sequence induction is performed with propofol, fentanyl, and succinylcholine.

The succinylcholine molecule consists of two acetylcholine molecules linked to each other at the acetyl portion of the molecule. This structural similarity to the endogenous acetylcholine molecule accounts for its ability to exert effects similar to acetylcholine at nicotinic acetylcholine receptors. Nicotinic acetylcholine receptors exist in both neuronal and muscle forms. The receptors themselves are composed of five transmembrane subunits, which form a central cation pore. Clinically, succinylcholine acts on the muscle nicotinic acetylcholine receptors. It binds to these acetylcholine receptors at the neuromuscular junction, causing opening of the ion channel in the receptor and membrane depolarization leading to skeletal muscle fasciculations. This is followed by a rapid desensitization of the receptor and inactivation of the ion channels, preventing propagation of action potentials and manifesting clinically as flaccidity. Unlike the acetylcholine molecule, which is broken down in <1 ms, succinylcholine remains at the neuromuscular junction. This causes a neuromuscular blockade which lasts for about 5–10 min, until the succinylcholine molecule is metabolized [1].

Succinylcholine is normally broken down through hydrolysis by pseudocholinesterase (also known as plasma cholinesterase or butyrylcholinesterase) into succinylmonocholine and choline. Pseudocholinesterase is synthesized in the liver. There are many conditions that can lead to reduced plasma activity of this enzyme, including pregnancy, oral contraceptives, liver disease, uremia, malnutrition, or plasmapheresis. The decrease in plasma cholinesterase in these cases can lead to a slight increase in the duration of action of succinylcholine, which is generally clinically irrelevant. Obese patients have increased plasma cholinesterase activity [2].

The peak onset of a dose of 1–2 mg/kg is achieved in less than 60 s. The time to peak onset will be longer if lower doses are used. Spontaneous respirations and diaphragmatic contraction generally will resume after about 5 min. Full recovery of neuromuscular function is dose dependent, and is about 10–12 min after a dose of 1 mg/kg [2].

Mutations in the gene that codes for plasma cholinesterase can result in abnormal enzyme activity, and therefore prolonged duration of neuromuscular blockade following succinylcholine administration. Significant prolongation of succinylcholine’s activity occurs when an individual is homozygous for the abnormal allele. The incidence is estimated to be 1: 2000. More commonly, an individual may be heterozygous for the abnormal allele (incidence about 1:30). Patients who are homozygous can have a neuromuscular blockade lasting up to 2–6 h. In comparison, individuals who are heterozygous for the abnormal allele will have a slightly prolonged paralysis [3].

Dibucaine is a local anesthetic that is known to inhibit normal plasma cholinesterase by 80%. In individuals who are homozygous for the atypical plasma cholinesterase, the activity of the enzyme is only inhibited 20%. In individuals who are heterozygous inhibition is about 50–60%. The dibucaine number therefore reflects the levels of normally functioning plasma cholinesterase. It will not be affected by conditions that cause a decrease in the quantity of normal plasma cholinesterase (i.e., liver disease, pregnancy). It is, in other words, a qualitative rather than quantitative test [3].