Prolonged Paralysis Caused by Plasmapheresis
Ed Mayo, MD
Department of Anesthesiology, University of Florida, Gainesville, FL
Case Report
Presentation: A 24-year-old woman was admitted to the hospital
for treatment of acute vascular rejection of a cadaveric renal
transplant secondary to a cytomegalovirus infection. During her
hospitalization, she sustained a calcium chloride infiltrate in
her upper extremity with significant tissue damage that
subsequently required two debridements. For her first
debridement, anesthesia was induced with sodium thiopental and
succinylcholine, 80 mg, to facilitate endotracheal intubation.
Anesthesia was maintained with O2, N2O, isoflurane, and fentanyl.
The surgery proceeded uneventfully and no anesthetic
complication was noted. For her second debridement, anesthesia
was again induced with sodium thiopental, but mivacurium, 13 mg,
was injected to facilitate endotracheal intubation. Fentanyl,
N2O, O2 and isoflurane were used for anesthetic maintenance.
Following conclusion of her surgery and anesthesia of
approximately one-hour duration, no respiratory efforts were
noted. In addition, no response to a “train of four” peripheral
nerve stimulus could be elicited. She was transferred to the
intensive care unit and mechanically ventilated overnight with
sedation. The subsequent day, she had resolution of her
neuromuscular blockade and was successfully extubated.
Discussion: Anesthesiologists caring for this patient noted that
her findings appeared similar to those of pseudocholinesterase
deficiency. However, no prolonged paralysis was noted during her
first surgery when succinylcholine was used. This depolarizing
neuromuscular antagonist is metabolized by pseudocholinesterase
and would be expected to cause prolonged paralysis in a patient
with this genetic disorder. However, between surgeries this
patient had underwent three episodes of plasmapheresis for
treatment of her acute vascular renal rejection of the renal
graft. Based on this information, a provisional diagnosis of
plasma cholinesterase deficiency was hypothesized. Follow up
laboratory examinations confirmed this diagnosis. Plasma
cholinesterase levels at the time were reduced to 867 IU/L
(normal 4970-11,120 IU/L) with a normal dibucaine (82.1) number.
This clinical and laboratory constellation strongly suggests
that whereas the patient had genetically normal enzymes,
plasmapheresis had markedly reduced cholinesterase
concentrations to levels insufficient to normally metabolize
mivacurium.
