Acute visual loss and pituitary apoplexy after surgery
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《英国医生杂志》
1 Birmingham and Midland Eye Centre, Birmingham B18 7QH
Correspondence to: J Abbott abbottjoseph@yahoo.com
Introduction
The exact pathophysiology of pituitary swelling in apoplexy is uncertain, but, histologically, ischaemic necrosis or haemorrhage is usually present or sometimes both.4
General anaesthesia and surgery, especially cardiac surgery, expose patients to risk factors for apoplexy of a pituitary tumour. These include embolisation, mechanical ventilation, labile blood pressure, coughing, anticoagulation, and crystalloid haemodilution.8-11 The cases presented are therefore representative of a population at risk of pituitary apoplexy.
Signs and symptoms of pituitary apoplexy result from acute compression of perisellar structures, endocrinopathy, and meningeal irritation.
Four in five patients present with a visual field defect, but, contrary to popular teaching, only half have a bitemporal hemianopia.4 Our first patient was not unusual in having one eye more profoundly affected than the other. This was due to asymmetrical compression of the chiasm and optic nerves.
We could not formally quantify the visual field defects because the patients were too unstable to leave their beds and too unwell to give reliable results in such investigations. This problem is likely to be seen often in patients who have recently had major surgery. Simple bedside examination of visual acuity, pupil reactions, and visual fields can be enough to identify the underlying pathology.
Ophthalmoplegia is a useful sign in conjunction with a sellar mass because it indicates apoplexy rather than a simple adenoma. This is caused by the mass having extended laterally into the cavernous sinus. Three quarters of apoplexy cases present with an eye movement abnormality,2 but this was absent in our cases.
Recognising that acutely expansile pituitary lesions may not cause papilloedema or optic atrophy is important. The discs were normal in both of our cases.
A pituitary mass may compromise hypothalamic function leading to impaired regulation of blood pressure, temperature, cardiac rhythm, and level of consciousness. These changes may be falsely attributed to the iatrogenic effects of surgery and general anaesthesia.
In patients with reduced consciousness it may not be possible to get a history of endocrine dysfunction. Amenorrhoea, gynaecomastia, impotence, and weight gain should specifically be asked about. Symptoms of endocrinopathy have been found in over a third of cases of pituitary apoplexy.2 5 We discovered a history of endocrine dysfunction in case 2 only when the patient had recovered from the acute illness.
In case 1 we found hyponatraemia—an important biochemical clue of endocrinopathy—present in 75% of patients at presentation.6 This probably reflects an established adrenocorticotrophic hormone deficiency and hypoaldosteronism.
Meningeal irritation caused by extravasated blood in the subarachnoid space can lead to diagnostic confusion. The commonest misdiagnosis is an intracranial aneurysm with subarachnoid haemorrhage.4 The differential diagnosis includes meningitis, cerebrovascular accident, cerebral metastatic disease, cavernous sinus thrombosis, and transtentorial herniation. The key to diagnosis is appropriate diagnostic suspicion prompting early neuroimaging and urgent hormonal assessment.
Patients who have recently had major surgery are at increased risk of pituitary apoplexy. They are particularly difficult to diagnose correctly and a delay in diagnosis and treatment is likely to adversely affect their outcome. This particularly applies to visual pathway compression where permanent visual damage is more likely if decompression is delayed.1 2 12 In the cases reported here visual acuity was improved from levels suitable for blind registration to almost normal.
Prompt recognition of pituitary apoplexy after major surgery allows endocrinological support and sight saving neurosurgery
We thank I Wilson and JAC Buckels for access to case notes and the initial referrals and also EB Rolfe for the image. AR Walsh and GS Cruikshank did the neurosurgery. P Stewart managed the endocrinopathy in case 2 and we are grateful for his advice regarding the final article.
Contributors: GRK was the examining ophthalmologist in both cases. JA wrote the initial draft document and both authors jointly produced the final article. GRK is guarantor.
Funding: None.
Competing interests: None declared.
References
Randeva HS, Schoebel J, Byrne J, Esiri M, Adams CBT, Wass JAH. Classical pituitary apoplexy: clinical features, management and outcome. Clin Endocrinol (Oxf) 1999;51: 181-8.
Bills DC, Meyer FB, Laws ER, Davis DH, Ebersold MJ, Scheithauer BW, et al. A retrospective analysis of pituitary apoplexy. Neurosurgery 1993;33: 602-9.
Sanno N, Teramoto A, Osamura, RY, Horvath E, Kovacs K, Lloyd RV, et al. Pathology of pituitary tumours. Neurosurg Clin N America 2003;14: 25-39.
McFadzean RM, Doyle D, Rampling R, Teasdale E, Teasdale G. Pituitary apoplexy and its effect on vision. Neurosurgery 1991;29: 669-75.
Ahmed M, Al-Jurf M. Pituitary apoplexy revisited. Arch Intern Med. 1993;153: 2165-8.
Vidal E, Cevallos R, Vidal J, Ravon R, Moreau J, Rogues A, et al. Twelve cases of pituitary apoplexy. Arch Intern Med. 1992;152: 1893-9.
Thorner MO, Vance ML, Laws ER, Horvath E, Kovacs K. In: Wilson JDM, Foster DWF, Kronenberg HM, Larsen PR, eds. Williams textbook of endocrinology. 9th ed. Philadelphia: WB Saunders, 1998.
Tang-Wai DF, Wijdicks EFM. Pituitary apoplexy presenting as postoperative stupor. Neurology 2002;58: 500-1.
Meek EN, Butterworth J, Kon ND, Zvara DA, Ash GE, Martin TJ. Pituitary apoplexy following mitral valve repair. Anaesthesiology 1998;89: 1580-2.
Alzetani A, Fisher C, Costa R, Ohri SK. Ptosis postcardiac surgery: a case of pituitary apoplexy. Ann Thorac Surg 2002;73: 300-1.
Cooper DM, Bazaral MG, Furlan AJ, Sevilla E, Ghattas MA, Sheeler LR, et al. Pituitary apoplexy: a complication of cardiac surgery. Ann Thorac Surgery 1986;41: 547-50.
Cardoso ER, Peterson EW. Pituitary apoplexy: a review. Neurosurgery 1984;14: 363-73.(Joseph Abbott, senior hou)
Correspondence to: J Abbott abbottjoseph@yahoo.com
Introduction
The exact pathophysiology of pituitary swelling in apoplexy is uncertain, but, histologically, ischaemic necrosis or haemorrhage is usually present or sometimes both.4
General anaesthesia and surgery, especially cardiac surgery, expose patients to risk factors for apoplexy of a pituitary tumour. These include embolisation, mechanical ventilation, labile blood pressure, coughing, anticoagulation, and crystalloid haemodilution.8-11 The cases presented are therefore representative of a population at risk of pituitary apoplexy.
Signs and symptoms of pituitary apoplexy result from acute compression of perisellar structures, endocrinopathy, and meningeal irritation.
Four in five patients present with a visual field defect, but, contrary to popular teaching, only half have a bitemporal hemianopia.4 Our first patient was not unusual in having one eye more profoundly affected than the other. This was due to asymmetrical compression of the chiasm and optic nerves.
We could not formally quantify the visual field defects because the patients were too unstable to leave their beds and too unwell to give reliable results in such investigations. This problem is likely to be seen often in patients who have recently had major surgery. Simple bedside examination of visual acuity, pupil reactions, and visual fields can be enough to identify the underlying pathology.
Ophthalmoplegia is a useful sign in conjunction with a sellar mass because it indicates apoplexy rather than a simple adenoma. This is caused by the mass having extended laterally into the cavernous sinus. Three quarters of apoplexy cases present with an eye movement abnormality,2 but this was absent in our cases.
Recognising that acutely expansile pituitary lesions may not cause papilloedema or optic atrophy is important. The discs were normal in both of our cases.
A pituitary mass may compromise hypothalamic function leading to impaired regulation of blood pressure, temperature, cardiac rhythm, and level of consciousness. These changes may be falsely attributed to the iatrogenic effects of surgery and general anaesthesia.
In patients with reduced consciousness it may not be possible to get a history of endocrine dysfunction. Amenorrhoea, gynaecomastia, impotence, and weight gain should specifically be asked about. Symptoms of endocrinopathy have been found in over a third of cases of pituitary apoplexy.2 5 We discovered a history of endocrine dysfunction in case 2 only when the patient had recovered from the acute illness.
In case 1 we found hyponatraemia—an important biochemical clue of endocrinopathy—present in 75% of patients at presentation.6 This probably reflects an established adrenocorticotrophic hormone deficiency and hypoaldosteronism.
Meningeal irritation caused by extravasated blood in the subarachnoid space can lead to diagnostic confusion. The commonest misdiagnosis is an intracranial aneurysm with subarachnoid haemorrhage.4 The differential diagnosis includes meningitis, cerebrovascular accident, cerebral metastatic disease, cavernous sinus thrombosis, and transtentorial herniation. The key to diagnosis is appropriate diagnostic suspicion prompting early neuroimaging and urgent hormonal assessment.
Patients who have recently had major surgery are at increased risk of pituitary apoplexy. They are particularly difficult to diagnose correctly and a delay in diagnosis and treatment is likely to adversely affect their outcome. This particularly applies to visual pathway compression where permanent visual damage is more likely if decompression is delayed.1 2 12 In the cases reported here visual acuity was improved from levels suitable for blind registration to almost normal.
Prompt recognition of pituitary apoplexy after major surgery allows endocrinological support and sight saving neurosurgery
We thank I Wilson and JAC Buckels for access to case notes and the initial referrals and also EB Rolfe for the image. AR Walsh and GS Cruikshank did the neurosurgery. P Stewart managed the endocrinopathy in case 2 and we are grateful for his advice regarding the final article.
Contributors: GRK was the examining ophthalmologist in both cases. JA wrote the initial draft document and both authors jointly produced the final article. GRK is guarantor.
Funding: None.
Competing interests: None declared.
References
Randeva HS, Schoebel J, Byrne J, Esiri M, Adams CBT, Wass JAH. Classical pituitary apoplexy: clinical features, management and outcome. Clin Endocrinol (Oxf) 1999;51: 181-8.
Bills DC, Meyer FB, Laws ER, Davis DH, Ebersold MJ, Scheithauer BW, et al. A retrospective analysis of pituitary apoplexy. Neurosurgery 1993;33: 602-9.
Sanno N, Teramoto A, Osamura, RY, Horvath E, Kovacs K, Lloyd RV, et al. Pathology of pituitary tumours. Neurosurg Clin N America 2003;14: 25-39.
McFadzean RM, Doyle D, Rampling R, Teasdale E, Teasdale G. Pituitary apoplexy and its effect on vision. Neurosurgery 1991;29: 669-75.
Ahmed M, Al-Jurf M. Pituitary apoplexy revisited. Arch Intern Med. 1993;153: 2165-8.
Vidal E, Cevallos R, Vidal J, Ravon R, Moreau J, Rogues A, et al. Twelve cases of pituitary apoplexy. Arch Intern Med. 1992;152: 1893-9.
Thorner MO, Vance ML, Laws ER, Horvath E, Kovacs K. In: Wilson JDM, Foster DWF, Kronenberg HM, Larsen PR, eds. Williams textbook of endocrinology. 9th ed. Philadelphia: WB Saunders, 1998.
Tang-Wai DF, Wijdicks EFM. Pituitary apoplexy presenting as postoperative stupor. Neurology 2002;58: 500-1.
Meek EN, Butterworth J, Kon ND, Zvara DA, Ash GE, Martin TJ. Pituitary apoplexy following mitral valve repair. Anaesthesiology 1998;89: 1580-2.
Alzetani A, Fisher C, Costa R, Ohri SK. Ptosis postcardiac surgery: a case of pituitary apoplexy. Ann Thorac Surg 2002;73: 300-1.
Cooper DM, Bazaral MG, Furlan AJ, Sevilla E, Ghattas MA, Sheeler LR, et al. Pituitary apoplexy: a complication of cardiac surgery. Ann Thorac Surgery 1986;41: 547-50.
Cardoso ER, Peterson EW. Pituitary apoplexy: a review. Neurosurgery 1984;14: 363-73.(Joseph Abbott, senior hou)