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An unusual presentation of a pituitary tumour in the early postpartum period.


The case of a parturient, who first presented with a partial oculomotor nerve palsy shortly after caesarean delivery while participating in a clinical trial, is presented. The anaesthesia for the caesarean delivery involved a combined spinal-epidural with intrathecal bupivacaine and postoperative epidural pethidine patient-controlled analgesia. The trial was examining the possible effects of magnesium infusions on acute and chronic pain. The partial oculomotor nerve palsy was an unusual presentation and the signs and symptoms were transient. Magnetic resonance imaging confirmed the presence of a presumed pituitary macroadenoma. Possible reasons for the timing of onset and the rapid resolution of symptoms, and the implications and management of pituitary pathology in the peripartum period, are considered. The uncomplicated course of a later caesarean delivery in the same patient, using the same anaesthesia technique, is also noted.

Key Words: pituitary tumour, postpartum


Pituitary adenomas represent the most common pituitary disorder affecting pregnancy (1). Although there are many reports of such tumours in the literature, initial presentation with oculomotor nerve palsy is uncommon (2-4) and does not appear to have been reported in a parturient. In addition, this case is unusual in that the postpartum presentation occurred during a period of increased surveillance because of the patient's involvement in a clinical trial.


The patient consented to the preparation of this manuscript for possible publication.

A 21-year-old nulliparous woman weighing 57 kg was admitted to our tertiary referral hospital for an elective caesarean section at 38 weeks gestation, the indication being breech presentation. She had no significant past medical or surgical history, was not on medication, the course of her pregnancy had been uneventful and haemoglobin concentration was 140 g/l.

She was recruited to an institution-approved research trial, comparing the effect of a perioperative infusion of magnesium or placebo on acute and chronic pain. The trial protocol involved the intravenous administration of study solution (saline placebo or one of two dosage regimens for magnesium, either 2g followed by 1 g/hour or 4g followed by 2 g/hour), the loading dose given over 30 minutes, starting one hour before surgery, with the maintenance dose continued for 24 hours. Her baseline serum magnesium concentration was 0.67 mmol/l (normal range 0.71.1 mmOl/l).

Anaesthesia was established using a combined spinal-epidural technique (16 gauge Tuohy needle and 27 gauge pencil-point spinal needle) with 2.5 ml of 0.5% hyperbaric bupivacaine and 10 [micro]g of fentanyl. The anaesthesia procedure was straightforward and the patient had a pain-free and uneventful 45-minute operation. A healthy 3105g infant was delivered and the estimated blood loss was 300 ml. The postoperative analgesic regimen was that most commonly used in this institution, namely patient-controlled epidural pethidine (20 mg bolus, 15 minute lockout), with regular paracetamol and a nonsteroidal anti-inflammatory drug commenced 24 hours postoperatively. The patient was monitored from baseline with respect to pain scores, sedation, respiratory rate, and tendon reflexes. Her initial postoperative course was unremarkable.

At approximately 22 hours postoperatively, the nursing staff noted her left eyelid to be drooping and requested the obstetric resident review the patient. The resident consulted the anaesthetic registrar and at 23 hours postoperatively her study infusion, which had been running for 21 hours, was ceased. During this period she had self-administered 160 mg of epidural pethidine. Four hourly monitoring of her tendon reflexes postoperatively had shown scores of 2+ (average response; normal) throughout. Her baseline rating had been 3+ (brisker than average; may not be abnormal). A serum magnesium assay revealed a concentration of 1.31 mmol/l, as a consequence of which the trial assignment code was not broken. A brief neurological examination showed left ptosis and a dilated left pupil that reacted slowly to light. Lateral movement of the eye was normal and other movements were present but upward gaze appeared to fatigue. She had not experienced headache, visual disturbance, facial muscle weakness, or sensory changes. She was afebrile and examination of the upper and lower limbs was normal.

On further questioning, the patient divulged that she had noticed drooping of her eyelid and an episode of blurred vision about 24 hours prior to hospital admission. Her mother stated that she had observed drooping of the left eyelid about four days previously. A diagnosis of oculomotor nerve palsy was considered and to investigate possible cavernous sinus pathology, the patient was transferred to another hospital with facility for magnetic resonance imaging (MRI) and neurological assessment.

She gave no history of headache, polyuria or polydipsia. Her cardiovascular and respiratory examination was normal. Her visual acuity was 6/5 in both eyes and her visual fields full to confrontation. Her eye movements were normal except for incomplete adduction and fatigue of vertical movement on the left. There was left ptosis and anisicoria (with the left pupil 2 mm larger than the right). Fundoscopy was normal, and apart from the incomplete third nerve paresis, examination of all other cranial nerves was normal. The MRI showed a left-sided pituitary tumour, measuring 15 mm transversely by 12 mm cranio-caudally by 13 mm antero-posteriorly, consistent with a macroadenoma. The tumour was situated in the left side of the gland and bulged into the left cavernous sinus, displacing the left carotid artery, with possible extension above the cavernous carotid artery. There was erosion of the left dorsum sellae but no displacement or compression of the optic nerve or chiasma. The tumour appeared homogeneous, adenomatous and showed no evidence of haemorrhage.

The patient was observed, endocrinological investigation instituted and hydrocortisone 100 mg was given intravenously. All investigations proved normal, including blood glucose, urea and electrolytes, blood picture and coagulation studies, liver and thyroid function tests, and levels of growth, follicle stimulating, luteinising and insulin-like growth hormones. Her morning serum cortisol was normal, although her serum prolactin levels of 5,020 (and next day 3,700) mU/l were elevated (normal resting <420 mU/l). These levels were consistent with the stimulation associated with suckling and establishment of lactation. She was reviewed by both a neurosurgeon and endocrinologist and conservative management was recommended. By the morning of the next postoperative day, 24 hours after detection of her ptosis, the weakness was resolving. The patient was returned to our hospital and discharged on the fifth postoperative day.

A repeat MRI scan was performed after six weeks. This again showed a well-defined mass of about 10 mm diameter in the left pituitary. It had significantly reduced in size compared with the previous scan and there was no suprasellar component. Hormonal tests were normal, except her serum prolactin, which was mildly elevated at 1,100 mU/l but consistent with her continued breast-feeding. Her menses had returned.

She did not attend a scheduled Endocrinology outpatient appointment a month later, but did have both Neurology and Endocrinology reviews approximately nine months later. At that time she was well, there was no evidence of third nerve palsy or visual field defect and her investigations were normal. However, she reported an eight-week history of amenorrhoea and beta-human chorionic gonadotrophin assay confirmed pregnancy.

Fourteen months after the initial presentation, she presented for a repeat elective caesarean section. This was again conducted under combined spinal-epidural analgesia, using similar equipment and regimen. She had remained asymptomatic during the pregnancy, had received no further review and on this occasion her intraoperative and postoperative course were unremarkable.


This patient's clinical course was interesting due to the unusual features and circumstances of her presentation with an undiagnosed pituitary adenoma. The clinical sign of unilateral ptosis, of apparently acute onset in the early postpartum period, raised a number of possibilities. Horner's syndrome presents with ptosis and miosis, enophthalmos and anhydrosis, and was excluded on the basis of ipsilateral mydriasis and the absence of a high sensory or sympathetic block. Epidural pethidine in the subarachnoid space may produce a sensory and motor block (5), but the patient's response to pethidine patient-controlled epidural analgesia had been normal, with no sign of lower limb dysfunction. Early weakness from magnesium toxicity is normally detected when tendon reflexes become depressed, and toxicity most commonly arises as a consequence of reduced clearance of magnesium because of impaired renal function. In this case, significant magnesium toxicity was excluded by the preservation of normal tendon reflexes, and the mildly elevated serum magnesium. Thus the magnesium administration seems unlikely to have contributed to skeletal muscle weakness, especially in the absence of an underlying disorder, such as myasthenia gravis. Finally, in the absence of other intracranial pathology, oculomotor nerve palsy is a rare complication of spinal anaesthesia or inadvertent dural puncture. The incidence is unknown, but I was unable to identify any case reports in a Medline search and it is the abducens (sixth cranial nerve) that is affected in 95% of post-dural puncture cranial nerve palsies (6). It is possible that loss of cerebrospinal fluid (CSF) from the dural puncture for spinal anaesthesia contributed to the palsy, and that cessation of the leak and restoration of normal CSF volume coincided with resolution.

On reviewing the clinical history with the patient, it became apparent that the onset of clinical signs had predated delivery and entry into the clinical trial. A history of signs indicative of partial oculomotor (third cranial) nerve palsy was elicited, making intracranial pathology the most likely aetiology. The oculomotor nerve pierces the dura lateral to the posterior clinoid process and traverses the cavernous sinus, before dividing. In addition to parasympathetic communication with the ciliary ganglion it supplies the muscles of the eye, including the levator palpebrae superioris, except the superior oblique and lateral rectus. The patient presented with signs of partial paresis. She had ptosis and pupillary mydriasis, and had previously experienced diplopia, which results from limitation of eye movement and inability to accommodate, although her eye movements appeared normal.

The presumptive diagnosis of a pituitary tumour was confirmed on MRI, the preferred imaging technique for pituitary pathology. Pituitary adenomas are the most common pituitary disorder affecting pregnancy, and prolactinomas the most common hormone-secreting adenomas'. These tumours are usually benign and slow growing, and are classified as microadenomas or macroadenomas based on size (less than or greater than 10 mm in diameter). The hormonal milieu of pregnancy may result in significant growth of the latter in up to a quarter of cases (7). Pituitary tumours may cause local mass effects (hypopituitarism, headache or visual field defects as a result of extrasellar extension and compression of the optic chiasm) or they may invade local structures (leading to ophthalmoplegia, seizures or hemiparesis). Most macroadenomas remain asymptomatic, only a small proportion presenting with headache or visual field disturbance. Surgery is rarely required given the responsiveness of prolactinomas to suppression with bromocriptine and reduction in size after pregnancy'. In this case, without a tissue diagnosis and with serum prolactin levels of 3-5,000 mU/l, the tumour was most likely to have been a non-functional prolactinoma (8).

The most common clinical presentation of a macroadenoma is with either a visual field defect or hormonal dysfunction and only a few cases of presentation with oculomotor nerve palsy are described (2-4). The rapid resolution of symptoms in the early postpartum period was interesting. The most likely explanation is the rapid change in hormonal milieu that occurs within 24 hours of delivery, when concentrations of both oestrogen and progesterone decrease, which decreases the stimulation of prolactin-producing lactotroph cells and oestrogen receptors on some prolactinomas (9). A much less likely possibility is that resolution occurred because of a reduction in serum magnesium concentration following cessation of the study infusion. Although an elevated serum concentration indicated that the infusate contained magnesium sulphate (at the end of the trial noted to be magnesium sulphate 1 g/hour), in retrospect, the patient's symptoms appears to have predated entry into the study. Magnesium has well-known effects at the neuromuscular junction, by acting as an antagonist to calcium at the pre-synaptic membrane, thus reducing acetylcholine release, and secondarily by decreasing the effect of acetylcholine on the postsynaptic membrane. However, in the absence of other factors causing partial neuromuscular block, clinical muscle weakness is considered unlikely at serum concentrations less than 5 mmol/l (10). It could be argued that, given some degree of inhibition of the electromyogram at therapeutic concentrations (11) and reduction of respiratory reserve in preeclamptic women with serum concentrations of 1.5-2 mmol/l (12), a contribution to the presentation by increased plasma magnesium levels cannot be excluded.

After investigation of this patient's pituitary tumour, a conservative management policy was adopted. The macroadenoma was not hormone-secreting and prolactin levels were only modestly elevated. A much less likely pathological diagnosis in this case was lymphocytic hypophysitis, which can only be definitively distinguished from a macroadenoma by tissue biopsy, and which may also spontaneously regress after pregnancy (13).

The patient was not discouraged from breast-feeding, because there are no data to suggest that the stimulation of prolactin secretion causes tumour growth. The second MRI, at the end of the post-partum period, showed no evidence of pituitary enlargement and she subsequently had another pregnancy without complication. In the absence of raised intracranial pressure, there was no contraindication to the use of spinal anaesthesia in this subsequent pregnancy.

In summary, the case of a parturient with an unusual presentation of a presumed pituitary macroadenoma, near the time of delivery, has been presented. The diagnosis of a pituitary mass may have been missed, had initial presentation not coincided with her hospital care in the early postoperative period--a period during which she was being monitored for muscle weakness because of her participation in a clinical research trial.

Accepted for publication on October 10, 2005.


(1.) Molitch ME. Pituitary diseases in pregnancy. Semin Perinatol 1998; 22:457-470.

(2.) Johnson LN, Pack WL. Transient oculomotor nerve misdirection in a case of pituitary tumor with hemorrhage. Arch Ophthalmol 1988; 106:584-585.

(3.) Abe T, Yamamoto M, Taniyama M et al. Early palliation of oculomotor nerve palsy following gamma knife radiosurgery for pituitary adenoma. Eur Neurol 2002; 47:61-63.

(4.) Varma D, Tesha P, George N. Acute painful third nerve palsy: the sole presenting sign of a pituitary adenoma. Eye 2002; 16:792-793.

(5.) Ngan Kee WD. Intrathecal pethidine: pharmacology and clinical applications. Anaesth Intensive Care 1998; 26:137-146.

(6.) Nishio I, Williama BA, Williams JP Diplopia: A complication of dural puncture. Anesthesiology 2004; 100:158-164.

(7.) Molitch ME. Management of prolactinomas during pregnancy. J Reprod Med 1999; 44(S12):1121-1126.

(8.) Randeva HS, Davis M, Prelevic CM. Prolactinoma and pregnancy. BJOG 2000; 107:1064-1068.

(9.) Bevan JS, Burke CW, Esiri MM, Adams CBT Misinterpretation of prolactin levels leading to management errors in patients with sellar enlargement. Am J Med 1987; 82:29-32.

(10.) James MFM. Magnesium in obstetric anesthesia. Int J Obstet Anesth 1998; 7:115-123.

(11.) Ramanathan J, Sibai BM, Pillai R, Angel JJ. Neuromuscular transmission studies in preeclamptic women receiving magnesium sulfate. Am J Obstet Gynecol 1988; 158:40-46.

(12.) Ramanathan J, Sibai BM, Duggirala V, Maduska AL. Pulmonary function in preeclamptic women receiving MgS04. J Reprod Med 1988; 33:432-435.

(13.) Flanagan DE, Ibrahim AE, Ellison DW et al. Inflammatory hypophysitis-the spectrum of disease. Acta Neurochirurgica 2002; 144:47-56.

M. J. PAECH * School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia

* M.B., B.S., D.R.C.O.G., F.R.C.A., F.A.N.Z.C.A., F.F.P.M.A.N.Z.C.A., D.M.,

Professor of Obstetric Anaesthesia, School of Medicine and Pharmacology, University of Western Australia.

Address for reprints: Dr M. Paech, Department of Anaesthesia and Pain Medicine, King Edward Memorial Hospital for Women, 374 Bagot Rd, Subiaco, Western Australia 6008.
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Author:Paech, M.J.
Publication:Anaesthesia and Intensive Care
Date:Feb 1, 2006
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