[Succinylcholine neuromuscular blockade in a case of pseudocholinesterase variant]

Since there is little or no pseudocholinesterase at the motor end plate, the neuromuscular blockade by succinylcholine is terminated by its diffusion away from the end-plate into extracellular fluid. Pseudocholinesterase (ChE), therefore, influences the duration of action of succinylcholine (SCC) by controlling the rate of hydrolysis before it reaches the end-plate. SCC neuromuscular blockade can be prolonged in the presence of an atypical form of ChE. A 37 year old male with the deficiency of ChE activity underwent pancreatico-duodenectomy under neuroleptanesthesia. The mode, duration and treatments of neuromuscular blockade following succinylcholine (SCC) were studied using train-of-four (TOF). SCC was administered 6 times (total 170 mg) during the operation. Prolonged apnea was noted after the first intravenous injection of SCC (60 mg, 1 mg.kg-1). It was found that spontaneous resolution of the neuromuscular block had four phases and there was a pronounced fade of the TOF response. After the second injection of SCC (30 mg), a remarkable fade of the TOF was detected and the character of the block was considered to be a desensitizing block (phase II block). The block was treated by intravenous infusion of fresh frozen plasma (FFP) (400 ml) which contained ChE, at the rate of 231 +/- 56 IU/l/37 degrees C begun shortly after the fifth injection of SCC (20mg). The duration of the block was remarkably shortened but the recovery curves were almost unchanged, indicating the diffusion of SCC away from the end-plate and/or that receptor-channel is presumably slow. The neuromuscular blockade was fully reversed by additional injection of FFP (400 ml) before extubation.(ABSTRACT TRUNCATED AT 250 WORDS)