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| LETTER TO EDITOR |
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| Year : 2021 | Volume
: 69
| Issue : 1 | Page : 201-203 |
An Incidental Empty Sella Causing Acute Posterior Pituitary Hypofunction in a Patient Presenting for Neurosurgery
Neeraja Ajayan1, Unnikrishnan Prathapadas1, Ajay P Hrishi1, Prakash Nair2
1 Department of Anesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
2 Department of Neurosurgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
| Date of Submission | 01-Jun-2019 |
| Date of Decision | 20-Jun-2019 |
| Date of Acceptance | 20-Mar-2020 |
| Date of Web Publication | 24-Feb-2021 |
Correspondence Address:
Ajay P Hrishi
Department of Anesthesiology, 4th Floor, C Block, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum - 695 001, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.310093
How to cite this article:
Ajayan N, Prathapadas U, Hrishi AP, Nair P. An Incidental Empty Sella Causing Acute Posterior Pituitary Hypofunction in a Patient Presenting for Neurosurgery. Neurol India 2021;69:201-3 |
How to cite this URL:
Ajayan N, Prathapadas U, Hrishi AP, Nair P. An Incidental Empty Sella Causing Acute Posterior Pituitary Hypofunction in a Patient Presenting for Neurosurgery. Neurol India [serial online] 2021 [cited 2021 Apr 11];69:201-3. Available from: https://www.neurologyindia.com/text.asp?2021/69/1/201/310093 |
Sir,
A 54-year-old female patient weighing 60 kg with no comorbidities presented with a left-sided hearing loss, tinnitus, and chronic intermittent headache associated with nausea, and a history of surgical decompression for left vestibular schwannoma seven years back. Neurological examination revealed a left-sided facial nerve palsy, eighth cranial nerve palsy, and papilledema. Computed tomography (CT) brain imaging revealed 4.7 × 3.1 cm extra-axial lesion in the left CP angle causing rotation of brain stem and compressing third and fourth ventricle with hydrocephalus and an empty sella with the normal hypothalamus [Figure 1]. Magnetic resonance imaging (MRI) showed an empty sella filled with the cerebrospinal fluid (CSF) and the normal pituitary gland was seen flattened on the sellar floor [Figure 2]. There was no history suggestive of hypopituitarism nor did her clinical examination reveal the same. Blood investigations including the hormonal profile were within normal limits. She was diagnosed as a case of recurrent left vestibular schwannoma and was posted for craniotomy and decompression the next day after admission. She had not been started on any medications including steroids before the procedure. | Figure 1: Sagittal post-contrast computed tomography (CT) scan of the brain showing well.defined large heterogeneously enhancing lesion epicentered at the cerebellopontine angle causing mass effect on the brain stem. Also noted incidentally are features of empty sella with cerebrospinal fluid in the sella turcica (Arrow)
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 | Figure 2: Magnetic resonance imaging (MRI) mid-sagittal section (T1 with contrast) showing an empty sella with CSF (Arrow) and the flattened pituitary gland on the sellar floor
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On the day of surgery, she was premedicated with oral alprazolam 0.5 mg. In the operating room, routine monitoring comprising of electrocardiogram (ECG), noninvasive blood pressure (NIBP), and pulse oximetry (SpO2) were started and she underwent standard anesthesia induction with propofol 2–3 mg/kg, fentanyl 2–3 mcg/kg, and vecuronium 0.1 mg/kg. After tracheal intubation, she was ventilated with air:oxygen (50:50) mixture and anesthesia was maintained with sevoflurane 2% (MAC 0.7–0.9) and infusions of fentanyl at 1 mcg/kg/h and atracurium at 0.5 mg/kg/h. Invasive arterial line and central line access were obtained post-induction, and neurological monitoring of seventh and eighth cranial nerves was also initiated. Later, two h into the procedure, the patient developed hypotension not responding to fluid therapy and vasopressors [Table 1]. We had not initiated any osmotherapy or diuretics before the hypotensive episode. We had administered 1200 mL of iso-osmolar crystalloids (ringer lactate and normal saline) to replace the patient's urine output and losses till then. Pulse pressure variability was closely monitored throughout and was maintained below 12 throughout the surgery. Suspecting hypocortisolism, Inj hydrocortisone 200 mg IV was administered, but the hypotension persisted. At this juncture, we noticed that urine output was exceeding 5 mL/kg/h and blood investigation revealed serum osmolarity of 305 meq/L and serum sodium of 149 meq/L. We presumed diabetes insipidus (DI) as the etiology which was later confirmed by urine osmolarity of 290 meq/L and urine specific gravity of 1.002 [Table 1]. A concomitant posterior pituitary hypofunction was suspected, and vasopressin infusion was initiated at 5 mU/kg/h and titrated to the effect following which she became hemodynamically stable, and other vasopressors were tapered and stopped [Table 1]. Urine output subsequently reduced to 100–150 mL/h and serum sodium came down to 140–143 meq/L. Post-surgery, she was extubated, after assessment of the sensorium. Her urine output, serum sodium, and serum osmolality were followed up, and vasopressin infusion was continued for the first three days due to ongoing DI. Over the following three days, as her diabetes insipidus resolved, the vasopressin therapy was tapered and stopped. She was discharged on the seventh postoperative day. On her follow-up at 3 months after surgery, she was found to have no clinical or biochemical features of hormonal deficiency. | Table 1: Table depicting the perioperative hemodynamic and biochemical variables of the patient along with the vasopressor therapy administered
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| » Discussion | |  |
Empty sella syndrome is a rare disorder where the pituitary gland is shrunk or flattened, and the sella turcica is filled with CSF on imaging. Most individuals with empty sella syndrome do not have any associated symptoms, but they can present with hormonal deficiencies. Many pathogenetic hypotheses have been proposed, including a congenital deficiency of the sellar diaphragm, suprasellar factors such as chronically increased intracranial pressure (ICP) and pituitary related factors such as a reduction in its size thereby promoting the intrasellar extension of subarachnoid space.[1],[2],[3] Our patient was a case of recurrent vestibular schwannoma having chronic intracranial hypertension which could have played a crucial role in the causation of her primary empty sella syndrome. Anterior pituitary dysfunction is found in 25% to 30% of the cases, with hyperprolactinemia being the commonest presentation. The release of other anterior pituitary hormones such as gonadotrophin, thyrotrophin, or adrenocorticotropic hormone (ACTH) could also be affected. Our patient had no clinical or biochemical manifestations of anterior hypopituitarism.
Vasopressin deficiency is an uncommon manifestation of empty sella syndrome.[1],[2] The stress response to surgery includes various perturbations in the internal milieu, of which derangements in hormonal processes play an integral role. During surgical stress, the neural and hormonal afferents evoke the hypothalamo-pituitary-adrenocortical (HPA) axis resulting in the activation of the sympathetic response. The release of Corticotropin-Releasing Factor (CRF41) and vasopressin (AVP) from hypothalamic neurons into the pituitary portal blood facilitate the release of ACTH which stimulates the secretion of cortisol into the systemic circulation. Vasopressin is an essential hormonal component of the stress response and its demand increases during surgical stress or pain.[4] Occult posterior hypopituitarism as in empty sella syndrome can produce blunting of the stress response and diabetes insipidus because of vasopressin deficiency. In our patient, though baseline hormonal profile showed no features of hypopituitarism, she could have had a relative vasopressin deficiency during the period of surgical stress as manifested by the essential triad of diabetes insipidus comprising hypernatremia, hyperosmolarity, and polyuria. This could be because of the lack of reserve of the posterior pituitary hormones which got unmasked during the period of stress. In the post-surgical period, the DI resolved, because of the amelioration of stress response, thereby reducing the requirement of vasopressin. Another rationale for this clinical presentation could be the compression of the pituitary stalk caused by the raised ICP. Thus, the transport of vasopressin from the hypothalamus to the posterior pituitary through the stalk is hampered resulting in low vasopressin stores. The compression could have been relieved in the postoperative period as the ICP was normalized.
The overt diabetes insipidus in our patient could have been aggravated by the intraoperative steroid therapy. The AVP neurons are highly sensitive to the early inhibitory effects of glucocorticoids as evidenced by the increased water excretion noted in patients receiving glucocorticoid replacement therapy. There are case reports of the unmasking of a central diabetes insipidus in patients receiving glucocorticoids in conditions of hypopituitarism such as septo-optic dysplasia, neurosarcoidosis, and empty sella syndrome.[5],[6] In our case, during the initial phase of hypotension, we had suspected hypofunctioning of the anterior pituitary for which hydrocortisone was administered, which could also have exacerbated the relative vasopressin deficiency during the period of stress. Hyponatremia and the panhypopituitary state have been reported in a setting of empty sella syndrome, which is contrary to the clinical picture encountered in our patient.[7]
To conclude, in patients with empty sella syndrome, posterior pituitary dysfunction could be unmasked during periods of stress such as surgery and pain and can present as refractory hypotension. It will be beneficial if the anesthesiologist considers this also in the differential diagnosis while evaluating for etiologies of hypotension in this subset of patients.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| » References | | |
| 1. | Marinis LD, Bonadonna S, Bianchi A, Maira G, Giustina A. Primary empty sella. J Clin Endocrinol Metab 2005;90:5471-7.  |
| 2. | Agarwal JK, Sahay RK, Bhadada SK, Reddy VS, Agarwal MK. Empty sella syndrome. J Indian Acad Clin Med 2001;2:198-202. |
| 3. | Zagardo MT, Cail WS, Kelman SE, Rothman MI. Reversible empty sella in idiopathic intracranial hypertension: An indicator of successful therapy? Am J Neuroradiol 1996;17:1953-6. |
| 4. | Finnerty CC, Mabvuure NT, Ali A, Kozar RA, Herndon DN. The surgically induced stress response. J Parenter Enteral Nutr 2013;37:21S-9S. |
| 5. | Puri M, Azam A, Loechner KJ. Unmasking of partial diabetes insipidus during stress but not maintenance dosing of glucocorticoids in an infant with septo-optic dysplasia. Int J Pediatr Endocrinol 2011;2011:817954. |
| 6. | Chin HX, Quek TP, Leow MK. Central diabetes insipidus unmasked by corticosteroid therapy for cerebral metastases: Beware the case with pituitary involvement and hypopituitarism. J R Coll Physicians Edinb 2017;47:247-9. |
| 7. | Tripathi M, Sanjeev CC, Roy AK. Chasing hyponatraemia: Unusual presentation. Neurol India 2001;49:197-9. [ PUBMED] [Full text] |
[Figure 1], [Figure 2]
[Table 1]
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