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Br J Ophthalmol. 2007 February; 91(2): 127–128.
PMCID: PMC1857604

A problem! Now a solution?

Short abstract

Diplopia after cataract surgery

Ophthalmologists are, and should be, proud of the advances in cataract surgery and aphakic correction that have occurred over the past two decades. Today, cataract surgery is considered one of the most successful surgical procedures performed throughout the world. The resulting quality of vision is usually excellent and the complication rate reasonably low. One postoperative complication, diplopia, has been a subject of intense scrutiny of late.1,2,3,4,5,6 Although multiple causes of diplopia after cataract surgery have been described, most recent studies have emphasised the problem of extraocular muscle toxicity resulting from direct injection with a local anaesthetic at the time of surgery.1,2,3,4,5,6 Han et al7 reported a series of patients with postoperative diplopic after cataract surgery. The authors concluded that 50% of the cases were associated with either direct trauma or anaesthetic myotoxicity to the extraocular muscles. It is noteworthy that they emphasised that overactions of the injured muscles were much more common than underactions. The only other major cause of persistent diplopia after cataract surgery in this study was sensory strabismus (32%).

Conventional local anaesthetics such as bupivacaine cause considerable myotoxicity and neurotoxicity.8 This has been studied extensively in skeletal muscle, but to a lesser degree in extraocular muscle.9 After the injection of bupivacaine into skeletal muscle, there is a dramatic degeneration of muscle fibres accompanied by a moderate inflammatory response.10,11 Subsequently, satellite cells are activated to myoblasts and take part in a brisk regeneration process. Localised muscle hypertrophy results in the area of the original anaesthetic injection.12 A similar sequence of events has been documented in the extraocular muscle of rats injected with metivacaine.13 The ultrastructure of regeneration of extraocular muscle fibres differs little from the regeneration of skeletal muscle fibres under these circumstances.

The issue of myotoxicity related to local anaesthetics has been recognised by ophthalmologists for two decades.9 Many experts in strabismus have invoked it to explain cases of post‐cataract surgery diplopia, especially those with a primary vertical deviation.1,2,3,4,5,6,7,14,15 However, the usual hypothesis has been that injection of a local anaesthetic directly into an extraocular muscle results in almost immediate paresis, followed by contracture and restriction of the injured muscle.1,2,3,5,6,15,16 Focal thickening of the involved extraocular muscle can be seen on magnetic resonance imaging scans and has usually been attributed to segmental contracture and fibrosis.1,2,16 However, not all authors agree that fibrosis and contracture is the ultimate outcome of extraocular muscle injury by local anaesthetics.4 An alternative hypothesis is that the injection of local anaesthesia causes muscle degeneration, followed by functionally relevant hypertrophy of the affected muscle. This, in turn, results in overaction and strengthening of the previous injured muscle. Scott et al, (see page xxx) in this issue of the journal, suggest that this explanation is not only reasonable but also likely. Moreover, they emphasise that the alternative hypothesis that invokes secondary fibrosis and scarring as a fundamental process in the repair of the injured muscle has not yet been documented in any animal studies.18 This alternative hypothesis by Scott et al to explain the events surrounding the myotoxicity of extraocular muscles is in itself thought‐provoking and exciting. However, they have taken the idea one step further. They report treating a patient who had had previous strabismus surgery but who presented with a persistent 14‐prism dioptre esotropia. They chose to treat this patient by injecting the right lateral rectus muscle with bupivacaine 0.75%, thus inducing paresis of the right lateral rectus for 7 days. This, however, was followed by a period of improvement in lateral rectus function, and the elimination of the diplopic 33 days after treatment. Alignment remained normal at an additional evaluation 54 days after treatment. Magnetic resonance imaging showed a focal increase in the size of the injected right lateral rectus of 58% in the posterior area, with less change in the anterior portion of the right lateral rectus muscle. The authors suggest that physiological strengthening of the right lateral rectus muscle as a result of the hypertrophy induced by the local anaesthetic injury provided an effective treatment for the small‐angle esotropia in this patient. Although this is a single case, with only short‐term follow‐up, it is a remarkable report. If further studies confirm these findings, therapeutic strengthening of extraocular muscles in the management of strabismus may become a reality.

Many questions remain. Animal studies and future human trials will be necessary. Ultimately, local anaesthetic injections may not be necessary to induce this change. Many questions surrounding the report of Scott et al can be raised. However, the fundamental observations of this case are noteworthy and truly ground‐breaking. The authors and other investigators should be encouraged to study the possible therapeutic use of local anaesthetic injections into extraocular muscle for the treatment of some forms of strabismus.


Competing interests: None declared.


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