Anaesthesia for surgical decompression of the orbit in severe thyroid orbitiopathy

Abstract

Anaesthesia for surgical decompression of the orbit in severe thyroid orbitiopathy has rarely been reported in the literature. This review highlights patients’, anaesthetic and surgical factors of relevance. We carried out a retrospective analysis over a 3-year period of the records of 35 patients who had undergone surgical orbital decompression via a trans-lid approach under general anaesthesia. A total of 58 decompressions were performed on 35 subjects (26 women, 9 men; age range 34–76 years). Twenty-four patients had bilateral decompressions (seven had both sides performed simultaneously, whereas 17 had each side performed separately at least one month apart). Eleven required unilateral decompression only. Surgery was repeated on six occasions in four of the 35 patients. The main indications for surgery were compressive optic neuropathy (n = 17) and disfiguring proptosis (n = 19). Fourteen patients had more than one indication. Of the 35 patients, 33 had a history of hyperthyroidism whereas the remaining two were clinically and biochemically euthyroid. In all cases, T4/TSH levels were normal pre-operatively. Two thirds were smokers (the majority smoking 10–20 cigarettes/day). Pre-operative morbidities were as follows: diabetes mellitus (n = 5), chronic airflow limitation (n = 4), asthma (n = 4), hypertension (n = 4), obesity (n = 3), ischaemic heart disease (n = 2), arrhythmias (n = 2) and CVA (n = 1). Five had 2–3 comorbidities. Fifty-one percent were taking prednisolone pre-operatively (dose range 10–80 mg). Average duration of anaesthesia was 119 min for unilateral surgery and 184 min for bilateral surgery. In 88% of cases, balanced anaesthesia involved a volatile agent (isoflurane > sevoflurane > enflurane), O2 /N2 O mixture and either remifentanil or fentanyl ± morphine, whereas in the remaining 12% of cases remifentanil, target-controlled infusion of propofol and O2/air mixtures were used. Normotensive anaesthesia was used throughout. Intravenous acetazolamide was given on induction to reduce intraocular pressure. Subcutaneous local anaesthetic (bupivacaine with epinephrine) was infiltrated under the eyelid before starting surgery. Ketorolac and pethidine were given as adjuncts in 29% and < 1% of cases respectively. In 26% of cases, anticholinergic therapy was required for bradycardia resulting from orbital traction. Postoperatively, nausea and/or vomiting was absent in 93% of cases, 57% of whom had not had antiemetic therapy intraoperatively. Postoperative pain scores of zero were recorded in 88% of cases, with the use of simple analgesics (paracetamol/codeine) or no analgesics recorded in 43% and 36%, respectively (for the entire hospital stay). Discharge home was on the first postoperative day in 76% of cases. Significant peri-operative complications were as follows: one patient suffered a CVA two days postoperatively and a CSF leak developed intra-operatively in another case (this resolved within 24 h and according to protocol a lumbar drain was inserted). Infraorbital anaesthesia was experienced in five cases (9%) (with complete resolution of symptoms after several months) and diplopia developed (15%) or worsened (22%) overall in 37% of cases. In our experience, anaesthesia for surgical decompression of the orbit is generally safe, has a low incidence of postoperative pain and nausea and vomiting and requires only a short hospital stay. However, one must be aware of the need to provide anaesthesia of long duration, and of the high incidence of pre-operative morbidities, smoking and high-dose steroid therapy.