Kava (Piper methysticum)
Kava is a popular herbal anxiolytic and sedative.[73]
Because of its psychomotor effects, it was one of the first herbal medications expected
to interact with anesthetics. The kavalactones (i.e., kawain, dihydrokawain, methysticin,
dihydromethysticin, yangonin, and desmethoxyyangonin) appear to be the source of
kava's pharmacologic activity.[74]
Kava acts by potentiating γ-aminobutyric acid (GABA) inhibitory
neurotransmission.[75]
Kavalactones and pentobarbital
produce a synergistic effect on [3
H]muscimol binding to GABA. This effect
probably explains why kava increased barbiturate sleep time in laboratory animals.
[76]
[77]
Prolonged
sedation with alprazolam and kava
was reported in one patient.[78]
Although kava
may have abuse potential, whether long-term use can result in addiction, tolerance,
and acute withdrawal after abstinence has not been satisfactorily investigated.
With heavy use, kava produces kava dermopathy, characterized
by reversible scaly cutaneous eruptions. Increasing evidence of kava hepatotoxicity
has caused its withdrawal in some countries.[79]
This may have important implications in patients with hepatic dysfunction.
Plasma levels peak 1.8 hours after an oral dose, and the elimination
half-life of kavalactones is 9 hours.[74]
These
pharmacokinetic data and the possibility of potentiation of the sedative effects
of anesthetics suggest that kava should be discontinued at least 24 hours preoperatively.
