[Orbital-bony decompression in patients with dysthyroid orbitopathy--first Croatian experiences]

Dysthyroid orbitopathy or Graves's orbitopathy is an entity made of symptoms and signs found within ocular apparatus, orbit and adnexal tissue in patients with thyroid dysfunction. Orbital pathogenesis is based on organ-specific autoimmune reaction, resulting in extra ocular muscle dysfunction and retro bulbar tissue changes. These changes are characterized by different stages of orbital inflammation, swelling and passive congestion. No infiltrative or inactive stage of the disease is most commonly seen in younger population as mild, orbital inflammation, lid retraction, variable proptosis and retro bulbar discomfort. Infiltrative or active stage of the disease usually affects older people and is characterized by a broad spectrum of clinical symptoms such as moderate or severe orbital inflammation, retro bulbar pain, lid retraction, periocular edema, proptosis with corneal exposure, extra ocular muscle dysfunction, conjunctival and episcleral congestion and optic nerve compression with loss of visual acuity. The current treatment concept for dysthyroid orbitopathy is to achieve euthyroidism with antithyroid drugs, radioiodine and thyroidectomy. Subsequently, for the treatment of dysthyroid orbitopathy immunosuppressive drugs such as corticosteroids, cyclophosphamide, methotrexate, cyclosporine, octreotides, orbital radiotherapy and surgical decompression can be used. Indications for orbital decompression are differentiated as urgent and elective. Current opinion is that only severe proptosis with corneal exposure and damage and compressive optic neuropathy urge orbital bony decompression combined with aggressive medical treatment. Persistent, active orbitopathy, retro bulbar discomfort or pain and disfiguring proptosis are indications for elective orbital bony decompression. Orbital bony decompression is a surgical method based on principle of opening the confined orbital bony space and allowing herniation of orbital fat into paranasal sinuses, thus decreasing orbital pressure.

A series of patients surgically treated for dysthyroid orbitopathy from July 2004 till November 2005, were followed-up. The group included 8 patients previously treated for thyroid dysfunction. Five patients (10 eyes) were operated on by the "swinging eyelid" approach (group 1) and three patients (6 eyes) by "inferomedial approach" (group 2). In group 1 proptosis reduction occurred in all patients, varying from 4 to 6 mm within 6-10 months postoperatively; retrobulbar pain or discomfort decreased in all patients few days after the surgery; and 2 patients still felt numbness in the n. infraorbitalis innervation area at 10 months of follow up. In group 2, all patients had proptosis reduction by 3-4 mm within 6-10 months postoperatively; retro bulbar discomfort disappeared in all patients a few days after the surgery. In this group none of the patients complained of infraorbital numbness 6 months of the surgery. All patients filled out a brief questionnaire before and 4 months after the surgery, ranking their symptoms and complaints.

Our patient series was rather small and selected, the data obtained are not representative of larger series. Based on these preliminary results and current literature data, we believe that orbital bony decompression is a highly effective, safe and quick procedure, easily adjustable to the surgeon as well as to the patient in achieving optimal results. We also believe that there is a need of better education of our patients considering the disease itself and treatment modalities through patient support groups or better physician-patient-nurse communication.