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Ann Thorac Surg 2002;73:300-301
© 2002 The Society of Thoracic Surgeons

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Case report

Ptosis postcardiac surgery: a case of pituitary apoplexy

^a Wessex Cardiac Centre, Southampton General Hospital, Southampton, United Kingdom

Accepted for publication May 1, 2001.

* Address reprint requests to Mr Ohri, Wessex Cardiac Centre, Southampton General Hospital, Tremona Rd, Southampton SO16 6YD, United Kingdom
e-mail: sohri.rph{at}excite.co.uk

	Abstract

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We present a patient in whom ptosis and third cranial nerve palsy developed postcoronary artery bypass grafting, and discuss the management of pituitary apoplexy postcardiac surgery.

	Introduction

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Pituitary apoplexy is the result of acute infarction, hemorrhage or edema of a preexisting pituitary adenoma. The resulting sudden expansion causes compression of the surrounding structures and this may lead to visual field defects or blindness, oculomotor palsies, headache, or even coma. These clinical presentations are often combined with endocrinological abnormalities due to pituitary gland injury.

A 72-year-old man presented for redo coronary artery bypass grafting (CABG) having undergone previous CABG in 1988. He represented with angina in 1997, and cardiac catheterization showed blocked vein grafts and a patent left internal thoracic artery (LITA) to left anterior descending artery (LAD). At the time of referral, he was in New York Heart Association class IV. He was referred for redo CABG on June 24th, 1998. His previous medical history was only notable for the presence of hypercholesterolemia. His physical examination was unremarkable.

At surgery, his vein grafts were occluded but the LITA to LAD was patent. The target vessels were poor, and he had a single graft to the distal right coronary artery and needle trans-myocardial revascularization to the obtuse marginal territory. The total bypass time was 45 minutes with no periods of ischemia (no aortic cross-clamp applied), the lowest mean blood pressure during cardiopulmonary bypass was 50 mmHg, and the lowest temperature was 32°C. Postoperatively, he was stable hemodyamically and was extubated the same day. On return to the ward, he complained of discomfort in his left eye and a left frontal headache. It was noted then that he had slight drooping of his left eyelid.

The next morning (day 2 postop) his discomfort and headache had resolved but developed complete ptosis of his left eyelid with edema. A neuroophthalmological review found absence of his levator function. The eye was looking down and out with no adduction, elevation, or depression. The pupil was dilated with poor reaction to light. A diagnosis of isolated third cranial nerve palsy was made, and the cause was suspected to be a small brain stem cerebrovascular injury.

He later developed pyrexia, hypotension, and his urine output was poor with no evidence of infection. He also had dysphagia and was noted to have an absent gag reflex with poor left palatal movement. He was generally weak and in constant nausea which was unresponsive to antiemetics. He was resuscitated with intravenous fluids and subsequently commenced on total parenteral nutrition.

Dexamethasone was given for his cranial nerve injury which also improved his general status. Parenteral feeding was switched to enteral feed through a fine-pore nasogastric tube. A computed tomographic scan was performed, and this showed an enlarged pituitary fossa filled with a soft tissue mass extending into the sphenoid air cells mainly on the left. Further imaging with magnetic resonance imaging (MRI) revealed a pituitary macroadenoma with suprasellar extension and evidence of hemorrhage suggesting infarction of a preexisting tumor (Fig 1).

View larger version (175K): [in this window] [in a new window]   Fig 1. Magnetic resonance imaging of sagittal section through the pituitary fossa showing the mass (arrow) occupying the whole of the fossa.

Conservative management was subsequently employed because the patient was clinically improving and did not wish to undergo any further surgical intervention. He was discharged 22 days postop in good general health, but with no sign of any resolution of his third nerve palsy. A repeat MRI 3 months postsurgery showed considerable shrinkage of the mass. On follow-up at 4 months, he was found to be active, walking 3 miles a day without cardiac complaint. He was noted to have reduced facial and body hair, and gynecomastia, which was treated with testosterone patches. His left ptosis was resolving and he had normal eye movement although he experienced diplopia on upward gaze.

	Comment

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The mechanism of pituitary apoplexy is hemorrhage or infarction. This may occur either spontaneously or following various conditions such as anticoagulation, positive pressure ventilation, radiotherapy, treatment with endocrinological trophic agents, prolonged coughing, pregnancy after induction of ovulation with clomiphene, and trauma [1, 2]. Clinical manifestations can be neurological: headache, lethargy, confusion, obtundation, unilateral, ptosis, meiosis, ophthalmoplegia involving cranial nerves 3, 4, and 6 (generally complete), visual field deficits, and hemiparesis. Endocrinological deficits are variable: adrenal insufficiency with hypotension and syncope, hypothyroidism, and gonadotrophins deficiency. There have been several reports in the literature of pituitary apoplexy after cardiac surgery [3–5]; most were in previously silent tumors such as the presented case.

Several factors in cardiac surgery have been implicated including systemic anticoagulation, hypotension, positive pressure ventilation, edema, hemodilution, reduced tissue oxygenation, and embolization [5].

Kovacs and Yao looked at the pituitaries of 33 patients who had died within 10 days of major cardiac surgery and found that 5 showed ischemic necrosis (15.2%). The management of these cases has been controversial [3]. Early surgery has been advocated in some series [4, 5] to prevent progression to a fatal state and to restore any functional loss such as visual field defects. This has to be balanced against the increased risk of morbidity or mortality for such an early (24 hours to 2 weeks) intervention after major heart surgery.

In less severe presentations, such as ophthalmoplegia or ptosis, surgery is not urgently indicated. Patients may be closely monitored with regular computed tomographic scans to await resolution of edema and hematoma. However this must be tempered with the potential for incomplete recovery with intractable diplopia as a distressing sequel [6].

If neurosurgical intervention is indicated, the recommended approach to the pituitary is the trans-sphenoidal route. The limited view of the surrounding structures (cavernous sinuses and carotid arteries) poses a risk of bleeding which may be difficult to control, especially if the procedure is done early after cardiac surgery in the context of coagulopathy and abnormal platelet function [4]. For the reasons discussed above, a conservative approach was adopted in the presented case with a gratifying clinical outcome.

	References

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1. Reid R.K., Malachi E.Q., Yen S.S.C. Pituitary apoplexy: a review. Arch Neurol 1985;42:712-719.[Abstract/Free Full Text]
2. Rovit R.L., Fein J.M. Pituitary apoplexy: a review and reappraisal. J Neurosurg 1972;37:280-285.[Medline]
3. Kovacs K., Yao J. Pituitary necrosis following major heart surgery. Z Cardiol 1975;64:52-57.
4. Savage E.B., Gugino L., Starr P.A., Black P.M., Cohn L.H., Aranki S.F. Pituitary apoplexy following cardiopulmonary bypass: consideration for a staged cardiac and neurosurgical procedure. Eur J Cardiothorac Surg 1994;8:333-336.[Abstract]
5. Cooper D.M., Bazaral M.G., Furlan A.J., et al. Pituitary apoplexy: a complication of cardiac surgery. Ann Thorac Surg 1986;41:547-550.[Abstract]
6. Slavin M.L., Budabin M. Pituitary apoplexy associated with cardiac surgery. Am J Ophthalmol 1984;98:291-296.[Medline]

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Aiman Alzetani Robert Costa Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Alzetani, A. Articles by Ohri, S. K. Search for Related Content PubMed PubMed Citation Articles by Alzetani, A. Articles by Ohri, S. K. Related Collections Cardiac - other