Sir,

We report the case of a 77-year-old man who developed lid oedema, chemosis, and diplopia on two occasions following intravenous administration of disodium pamidronate.

Pamidronate,1 or aminobiphosphonate, is a potent inhibitor of osteoclastic bone resorption but does not inhibit bone formation. It is used in the control of hypercalcaemia of malignancy, and in the treatment of osteolytic lesions and bone pain associated with metastatic breast carcinoma and multiple myeloma. It is sometimes indicated in the management of Paget's disease of bone.2 Ocular side effects, including conjunctivitis, episcleritis, scleritis, and uveitis have been described in the literature.3 Although the manufacturer has confirmed rare reports of transient diplopia, we found no other cases in the published literature.

Our patient was given intravenous disodium pamidronate for treatment of osteolytic lesions secondary to multiple myeloma. On each occasion, he became symptomatic 2 days after receiving the treatment. He developed erythema and swelling of both upper lids, chemosis, and vertical diplopia, worse on upgaze. On the first occasion, he was assessed in the eye clinic several days after the onset of symptoms. Chemosis and conjunctival injection had begun to subside by the time of examination. He had a 1 mm left ptosis and bilateral limitation of upgaze, which affected the right eye more than the left. There was some limitation of abduction bilaterally. After 4 months, he received intravenous disodium pamidronate again. Eyelid oedema, chemosis, conjunctival injection, and diplopia developed within 48 h of administration, and again resolved spontaneously. The time course of onset and resolution were similar to the previously observed pattern. On review, 2 months later he was free of symptoms and ocular motility testing was normal. Vertical diplopia in the primary position recovered over the course of 2 weeks on each occasion, diplopia on elevation persisting for a further 2 weeks. Chemosis and lid oedema had resolved within 5 days of onset of each episode. No signs of uveitis were observed on either occasion.

Discussion

It is unclear why pamidronate should have a selective effect in inducing an inflammatory reaction in the orbital tissues, with no apparent effect on muscle function elsewhere in the body. It is probable that the intraorbital inflammation and consequent oedema involved the recti muscles during both the episodes. If the effects of intraorbital oedema on muscle function were not equal bilaterally, as is evident from Hess chart (Figure 1) recorded during the second episode, then diplopia during conjugate eye movements would be expected. Diplopia in the primary position may have been due to breakdown of a small pre-existing vertical phoria, although none was clinically evident when he was assessed after resolution of the second episode.

Figure 1
figure 1

Hess chart recorded following re-challenge with intravenous disodium pamidronate.

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