Fig. 6.1
Sagittal contrast-enhanced MRI (a) and CECT head (b) showing a giant pituitary adenoma with parasellar and subfrontal extensions. Figure (c) showing postoperative pituitary apoplexy in the residual tumour
Semple et al. (2008) correlated the MRI findings with the histopathological results to assess how accurately the histopathology was predicted by the MRI. When they compared the histopathological diagnosis with preoperative MRI findings, the histopathology correlated with the MRI in 68 % of patients with a histopathological diagnosis of haemorrhagic infarction/haemorrhage and in 82 % of patients with infarction alone (Semple et al. 2008). The histopathological diagnosis could therefore be equated with the MRI findings in the majority of cases, although the findings were less accurate in the haemorrhagic group (Semple et al. 2008).
6.6 Differential Diagnoses
Clinical conditions frequently misdiagnosed as pituitary apoplexy are subarachnoid haemorrhage due to ruptured intracranial aneurysm and meningitis. Other diseases that may have similar clinical characteristics are hypertensive encephalopathy, brain abscess or cyst, cavernous sinus thrombosis, intracerebral haematoma, basilar artery occlusion, encephalitis, retrobulbar neuritis, temporal arteritis and ophthalmoplegic migraine (Chang et al. 2009).
6.7 Discussion
Pituitary apoplexy is a dangerous condition, often characterized by acute onset of headache, nausea, visual field loss and ocular paresis (Bills et al. 1993; Randeva et al. 1999). Massive swelling and haemorrhage in a pituitary tumour or the phenomenon of “postoperative pituitary apoplexy” following a subtotal or a partial resection of giant pituitary adenomas was described by Goel et al. in 1995 (Goel et al. 1995). The senior author has also previously published a series of four cases of postoperative pituitary apoplexy (Ahmad et al. 2005). All the four patients in our series and in the series reported by Goel et al. (1995) had giant pituitary tumours. There was postoperative worsening in the neurological status in all the four reported cases. There was no evidence of alteration of coagulation parameters. Despite the decompression of the haemorrhagic tumour during the reoperations, all the patients had a stormy postoperative course and subsequently died.
In a recently published article, the senior author has presented our institute experience of managing postoperative pituitary apoplexy (Kurwale et al. 2012). Patients with postoperative pituitary apoplexy were critically reviewed for clinical presentation, endocrine status, preoperative imaging and postoperative course with outcome. Operative findings and histopathology were correlated. Thirteen patients over 11 years with a mean age of 36 years were reviewed. All patients had giant pituitary adenomas. Four patients had functional adenomas. All patients were optimized for endocrine status before surgery. Twelve patients underwent transsphenoidal excision of the tumour. Only partial excision could be achieved in all cases. Deterioration of consciousness (nine patients), visual deterioration (three patients), delayed reversal and excessive bleeding (one patient) were the primary indicators toward apoplexy. Ten patients were reexplored within 24 h of first surgery. All except one were explored transcranially a second time. Twelve patients died with variable postoperative course. Hypothalamic dysfunction and dyselectrolytaemia (nine patients) were leading causes of death, followed by meningitis and raised intracranial pressure. The authors concluded that postoperative pituitary apoplexy is associated with high mortality, despite early and best management (Kurwale et al. 2012). Partial resection of the giant pituitary adenoma is directly responsible for postoperative apoplexy. Maximum possible resection of the tumour by suitable exposure should be the optimal goal of surgery. Surgical exposure, either transcranial or transsphenoidal, should be dictated by tumour configuration on preoperative imaging. Endocrine status, histology of the tumour and clinical presentation do not appear to contribute to postoperative pituitary apoplexy.
6.8 Treatment
As soon as diagnosis of pituitary apoplexy is made and after collecting blood sample for haematological, biochemistry and hormonal analysis, glucocorticoids should be administered in supraphysiological doses to serve not only as replacement for endogenous hormone deficiency but also to help control the effect of oedema. Dose recommended is between 8 and 16 mg dexamethasone or hydrocortisone 50 mg intravenously every 6 h during the first 48 h (Chacko et al. 2002; Dubuisson et al. 2007). Occasionally, patients are clinically or biochemically hypothyroid at presentation, a factor to be considered prior to surgical intervention. However, hypothyroidism is not a contraindication for surgery (Chang et al. 2009).
If there is altered mental status without recovery after neurological and endocrinological treatment, surgical intervention is required (Chang et al. 2009). The choice of surgical approach has to be decided on a case to case basis. Surgical exposure, either transcranial or transsphenoidal, should be dictated by tumour configuration on preoperative imaging (Kurwale et al. 2012)
It is important to note that endocrinological follow-up after surgery is necessary since many patients need hormonal replacement for a long-term basis (Chang et al. 2009).
Conclusion
Postoperative pituitary apoplexy is associated with high mortality, despite early and best management. Partial resection of the giant pituitary adenoma is directly responsible for postoperative apoplexy. Maximum possible resection of the tumour should be the optimal goal of surgery. Surgical exposure, either transcranial or transsphenoidal, should be dictated by tumour configuration on preoperative imaging.
References
Ahmad FU, Pandey P, Mahapatra AK. Post operative ‘pituitary apoplexy’ in giant pituitary adenomas: a series of cases. Neurol India. 2005;53:326–8.PubMedCrossRef
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