Chapter 87 Bupivacaine injection of eye muscles to treat strabismus
Introduction
Botulinum toxin A
This drug weakens EOM. It was first used for strabismus in 1978; a large experience of its use has been reported since. Chapter 84 addresses this topic.
Bupivacaine
Mechanism of action
Small lipophilic local anesthetic molecules penetrate cell walls and attach to voltage gated sodium channels of nerves and muscles, blocking propagation of nerve and muscle action potentials. It is reversible and leaves no damage. BUP is especially lipophilic and strongly penetrates the sarcoplasmic reticulum of muscle fibers where it causes myotoxic damage by releasing the stored calcium into the cytosol and blocking calcium re-uptake by the sarcoplasmic reticulum. The high calcium concentration in the cytosol damages the mitochondria of the muscle fiber and activates an enzyme that dissolves the Z-band fibers of the muscle, resulting in separation of the sarcomeres.1–3 The damaged fibers are not repaired, but are removed over the next few days by macrophages leaving the cell membranes, nerves, and blood vessels intact.1–8 Within a few hours of exposure to BUP, autocrine growth factor molecules such as insulin growth factors IGF-I and IGF-IEc or mechano growth factor (MGF) are released from the damaged area. These molecules activate the satellite cells that are scattered around each muscle fiber. The satellite cells proliferate and coalesce to form new muscle fibers and myocytes to replace the damaged muscle, a process taking 3 weeks.1,4,7,9,10,11 In EOM, regeneration builds a muscle that has larger muscle fibers and is increased in size 5−10%, especially in its posterior third. The regenerated muscle is stiffer than before, probably due to added non-contractile fibrous tissue within the muscle.9,11,12 These biomechanical alterations change eye alignment.
An EOM treated with BUP appears to regenerate to the length at which it is held during the process of regeneration. Physically restraining the eye to do this is impractical. A small dose of Botox® to the antagonist to weaken it for 3−4 weeks prevents stretching of the BUP injected muscle during the phase of regeneration. This allows the BUP injected muscle to regenerate to a shorter length, doubling the correction effect as compared to use of BUP alone.13
