Serum potassium concentrations after suxamethonium in patients with familial amyloid polyneuropathy type I

Suxamethonium produces an abnormal increase in serum potassium in some neurological diseases and some authors have suggested that it is safer not to use this drug in patients with familial amyloid polyneuropathy (FAP). However, there are no data previously reported to support this hypothesis. The aim of this study was to evaluate the magnitude of the potassium increase produced by suxamethonium in FAP type I.

Twenty-one FAP Met 30 patients anaesthetised for liver transplantation were studied. Age was 34.9 +/- 6.9 years (mean +/- SD), time elapsed from first symptom 5.5 +/- 3.2 years and weight was 14 +/- 9% below ideal body weight. Anaesthesia was induced with thiopentone and low-dose fentanyl. Samples for blood gas and 5 min after 1 mg/kg of suxamethonium was given for tracheal intubation.

Before induction serum potassium levels were 3.8 +/- 0.4 mmol/L. One minute after suxamethonium, values were 3.8 +/- 0.4 mmol/L and 5 min after 4.3 +/- 0.5 mmol/L. The maximal increase observed was 1.6 mmol/L (from 3.4 mmol/L to 5.0 mmol/L).

The average increase in plasma potassium concentrations observed in FAP patients after suxamethonium was similar to the increase observed in a normal population by others. Our study can exclude the hypothesis that an anomalous increase in potassium would be a typical and frequent response to suxamethonium in FAP met 30 patients. However, we cannot exclude that a dangerous rise in serum potassium may exist in a certain percentage of FAP patients.