Certainly, other sources of the fungus are possibilities of a pituitary adenoma due to haemorrhage or infarction. and the authors postulate that a wick of anterior capsule Usually, pituitary apoplexy is accompanied by the in the wound probably acted as a nidus and a portal of sudden onset of headache with meningeal irritation, and entry. In any case early diagnosis with persistent and sustained antifungal therapy resulted in an extremely frequently followed by visual impairment and -4 ophthalmoplegia.l However, these symptoms may not favourable outcome. be present and therefore misdiagnosis of the disease frequently occurs. Such a delay in diagnosis may lead to References visual impairment because an early diagnosis and 1. Tabbara KF, Al Jabbarti AL. Hospital construction-associated subsequently surgical decompression of the sellar region outbreak of ocular aspergillosis after cataract surgery. Ophthalmology 1998;105:522-6. 2. Kwon-Chung KJ, Bennet J. Aspergillosis. In: Kwon-Chung KJ, Bennet J, editors. Medical mycology. Philadelphia: Lea & Feibiger, 1992:201-3, 219-23. 3. Valenton, M. Wound infection after cataract surgery. Jpn J Ophthalmol 1996;40:447-55. 4. Paulose KO, et al. Mycotic infection of the ear (otomycosis): a prospective study. J Laryngol Otol 1989;103:30-5. 5. Weishaar PD, Flynn HW Jr, Murray TG, Davis JL, Barr CC, Gross JG, et al. Endogenous Aspergillus endophthalmitis: clinical features and treatment outcomes. Ophthalmology 1998;105:57-65. 6. Graham DA, Kinyoun JL, George DP. Endogenous Aspergillus ophthalmitis after lung transplantation. Am J Ophthalmol 1995;119:107-9. 7. Hunt KE, Glasgow BJ. Aspergillus endophthalmitis: an unrecognised endemic disease in orthoptic liver transplantation. Ophthalmology 1996;103:757-67. within a few days of apoplexy is of major importance in 5 7 restoring vision and severe pituitary failure. Here we report a patient with an unusual presentation of pituitary apoplexy without headache or other general symptoms. The visual field deficit in both eyes was characterised as being chiasmatic and the CT scan led us to the correct diagnosis within 4 h. Case report An otherwise healthy 27-year-old man was referred to our hospital because of the acute onset of blurred vision. He denied any headache or double vision. He also denied any neurological or endocrinological symptoms. Ophthalmic examination showed a visual acuity of 20/20 8. Katz G, Winchester K, Lam S. Ocular aspergillosis isolated in the anterior chamber. Ophthalmology 1993;100:1815-9. Naveen K, Kermani, FRCSEd I2!'l in the right eye and 20/600 in the left. There was no improvement with pinhole. Ocular motility examination was normal. No intraocular abnormalities were seen in either eye and there was no relative afferent pupillary Shashi P. Aggarwal defect. Perimetry showed incomplete bitemporal Department of Ophthalmology Guest Hospital hemianopia (Fig. 1). A cerebral CT scan was immediately Tipton Road done and showed a sellar tumour with hypodense areas Dudley DYl 4SE as a sign of a haematoma (Fig. 2). Based on these findings West Midlands, UK the diagnosis of pituitary apoplexy was made and transsphenoidal decompression of the sellar region was Sir, performed 16 h after the patient had initially experienced Incomplete bitemporal hemianopia without headache: blurred vision. Surgery was performed without any an unusual case of pituitary apoplexy intraoperative complications. On the first post-operative Pituitary apoplexy is a well described but uncommon day visual acuity in the left eye improved to 20/30 and in clinical syndrome resulting from a sudden enlargement neither eye was any visual field defect noted (Fig. 3). " -.- . , � . ··=.�: :��·:iIJ;: '-' (a) _. (b) Fig. 1. Visual field before surgery showing an incomplete bitemporal hemianopia. (a) Right eye; (b) left eye. 116 . I the sellar region or abnormalities in ocular motility is of critical importance. A following CT scan permits the diagnosis of pituitary apoplexy. lD References 1. Millazzo S, Toussaint P, Proust F, Touzet G, Malthieu D. Ophthalmic aspects of pituitary apoplexy. Eur J Ophthalmol 1996;6:69-73. 2. Brougham M, Heusner AP, Adams RD. Acute degenerative (arrowed). changes in adenomas of the pituitary body: with special reference to pituitary apoplexy. J Neurosurg 1950;7:421-39. 3. Ahmed M, Rifai A, Aj-Jurf M, Akhtar M, Woodhouse N. Classical pituitary apoplexy: presentation and a follow-up of 13 patients. Hormone Res 1989;31:125-32. 4. Cardoso ER, Peterson EW. Pituitary apoplexy: a review. Neurosurgery 1984;14:363-73. 5. McFadzean RM, Doyle D, Rampling R, Teasdale E, Teasdale G. Pituitary apoplexy and its effect on vision. Neurosurgery Comment 6. Bills DC, Meyer FB, Laws ER, Davis DH, Ebersold MJ, Fig. 2. CT scan showing pituitary adenoma with haemorrhage 1991;29:669-75. The incidence of pituitary adenoma is around 15% of all symptomatic intracranial neoplasms. Although uncommon before the age of 20 years, their incidence increases with age after the fourth decade of life. Autopsy studies have shown that the prevalence of asymptomatic pituitary adenomas may be as high as 27% and that adenomatous hyperplasia may be found in almost every pituitary gland.s Pituitary apoplexy is a rare complication of pituitary adenoma with a frequency between 0.6% and 10% of operated adenomas.6,9 The classical clinical Scheithauer BW, et al. A retrospective analysis of pituitary apoplexy. Neurosurgery 1993;33:602-9. 7. Arafah BM, Harrington F, Madhoun ZT, Selman WR. Improvement of pituitary function after surgical decompression for pituitary tumor apoplexy. J Clin Endocrinol Metab 1990;71:323-8. 8. Burrow GN, Wortzman G, Rewcastle NB, et al. Microadenomas of the pituitary and abnormal sellar tomograms in an unselected autopsy service. N Engl J Med 1981;304:156-8. 9. Kaplan B, Day AL, Quisling R, Ballinger W. Hemorrhage into pituitary adenomas. Surg Neurol 1983;20:280-7. 10. Naidich TP, Pinto RS, Kushner MJ, Lin PI. Kricheff II, Leeds appearance of pituitary apoplexy with the sudden onset NE, Chase NE. Evaluation of sellar and parasellar masses by computed tomography. Radiology 1976;120:91-9. of headache, often accompanied by vomiting and signs of meningitis, is well recognised, but not always present. Therefore, misdiagnosis of apoplexy is not uncommon. A further cause for confusion is the absence of clinical features of an endocrinological disorder.3,4 Visual impairments are very common at clinical onset and are the most important clinical features of pituitary apoplexy. Depending on the location these visual impairments are shown as a visual field defect that characterises the lesion as being chiasmatic if the growth of the pituitary mass is superior or as ocular motility defects due to inferior growth and cavernous sinus compression.4 Therefore, for the correct diagnosis a careful demonstration of a visual field deficit related to (a) Chris P. Lohmann' Markus K6hler2 Odo-Winfried Ulirich2 'Department of Ophthalmology 2Department of Neurosurgery University of Regensburg Regensburg, Germany Dr Chris P. Lohmann, MD, PhD � Universitats-Augenklinik Franz-Josef-Strauss-Allee D-93042 Regensburg, Germany Tel: +49 941 9449201 Fax: +49 941 9449202 e-mail: chris.lohmann@klinik.uni-regensburg.de (b) Fig. 3. Visual field 1 day after decompression of the sellar region. No visual field defect was noted. (a) Right eye; (b) left eye. 117