sodilators [4, 5]. This procedure could be lifesaving asdemonstrated in the present report. Could the sequenceof distal grafting have been altered to improve theoutcome? This is difficult to answer, however, it is pref-erable to graft posterolateral circumflex artery branchesfirst in beating heart coronary revascularization to pre-vent any tension on the LITA to LAD anastomosis withthe required heart rotation toward the right chest. De-spite the fact that norepinephrine has the least coronaryartery vasoconstrictive effect compared with other com-monly used vasopressors, its constant administration tosupport a low blood pressure during off-pump coronarysurgery should lower the threshold for conversion tocardiopulmonary bypass assisted coronary artery bypassgrafting. In order to avoid additional catecholamine re-lease, stress responses, and hypoxemia-induced hemo-dynamic compromise with awakening in the operatingroom, operating table extubation should not have beenconsidered in this patient, which in combination withhigh doses of intravenous phenylephrine could have ledto the unexpected catastrophic event of coronary arteryvasoconstriction.

References

1. Pires LA, Wagshal AB, Lancey R, Huang SKS. Arrhythmiasand conduction disturbances after coronary artery bypassgraft surgery: epidemiology, management and prognosis. AmHeart J 1995;129:799–808.

2. Zeff RH, Iannone LA, Kongtahworn C, et al. Coronary arteryspasm following coronary artery revascularization. Ann Tho-rac Surg 1982;34:196–200.

3. Paterson HS, Jones MW, Baird DK, Huges CF. Lethal postop-erative coronary spasm. Ann Thorac Surg 1998;65:1571–3.

4. Lemmer JH, Kirsh MM. Coronary artery spasm followingcoronary artery surgery. Ann Thorac Surg 1988;46:108–15.

5. He G-W, Yue-Yan Fan K, Chiu S-W, Chow W-H. Injection ofvasodilators into arterial grafts through cardiac catheter torelieve spasm. Ann Thorac Surg 2000;69:625–8.

Ptosis Postcardiac Surgery: A Caseof Pituitary ApoplexyAiman Alzetani, FRCS, Christopher Fisher, MB, RobertCosta, FRACS, and Sunil K. Ohri, FRCS

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

We present a patient in whom ptosis and third cranialnerve palsy developed postcoronary artery bypass graft-ing, and discuss the management of pituitary apoplexypostcardiac surgery.

(Ann Thorac Surg 2002;73:300–1)© 2002 by The Society of Thoracic Surgeons

Pituitary apoplexy is the result of acute infarction,hemorrhage or edema of a preexisting pituitary

adenoma. The resulting sudden expansion causes com-pression of the surrounding structures and this may leadto visual field defects or blindness, oculomotor palsies,headache, or even coma. These clinical presentations areoften combined with endocrinological abnormalities dueto pituitary gland injury.

A 72-year-old man presented for redo coronary arterybypass grafting (CABG) having undergone previousCABG in 1988. He represented with angina in 1997, andcardiac catheterization showed blocked vein grafts and apatent left internal thoracic artery (LITA) to left anteriordescending artery (LAD). At the time of referral, he wasin New York Heart Association class IV. He was referredfor redo CABG on June 24th, 1998. His previous medi-cal history was only notable for the presence of hy-percholesterolemia. His physical examination wasunremarkable.

At surgery, his vein grafts were occluded but the LITAto LAD was patent. The target vessels were poor, and hehad a single graft to the distal right coronary artery andneedle trans-myocardial revascularization to the obtusemarginal territory. The total bypass time was 45 minuteswith no periods of ischemia (no aortic cross-clampapplied), the lowest mean blood pressure during cardio-pulmonary bypass was 50 mmHg, and the lowest tem-perature was 32°C. Postoperatively, he was stable he-modyamically and was extubated the same day. Onreturn to the ward, he complained of discomfort in hisleft eye and a left frontal headache. It was noted then thathe had slight drooping of his left eyelid.

The next morning (day 2 postop) his discomfort andheadache had resolved but developed complete ptosis ofhis left eyelid with edema. A neuroophthalmologicalreview found absence of his levator function. The eye waslooking down and out with no adduction, elevation, ordepression. The pupil was dilated with poor reaction tolight. A diagnosis of isolated third cranial nerve palsy wasmade, and the cause was suspected to be a small brainstem cerebrovascular injury.

He later developed pyrexia, hypotension, and his urineoutput was poor with no evidence of infection. He alsohad dysphagia and was noted to have an absent gagreflex with poor left palatal movement. He was generallyweak and in constant nausea which was unresponsive toantiemetics. He was resuscitated with intravenous fluidsand subsequently commenced on total parenteralnutrition.

Dexamethasone was given for his cranial nerve injurywhich also improved his general status. Parenteral feed-ing was switched to enteral feed through a fine-porenasogastric tube. A computed tomographic scan wasperformed, and this showed an enlarged pituitary fossafilled with a soft tissue mass extending into the sphenoidair cells mainly on the left. Further imaging with mag-netic resonance imaging (MRI) revealed a pituitary mac-roadenoma with suprasellar extension and evidence of

Accepted for publication May 1, 2001.

Address reprint requests to Mr Ohri, Wessex Cardiac Centre, Southamp-ton General Hospital, Tremona Rd, Southampton SO16 6YD, UnitedKingdom; e-mail: sohri.rph@excite.co.uk.

300 CASE REPORT ALZETANI ET AL Ann Thorac SurgPITUITARY APOPLEXY POSTCARDIAC SURGERY 2002;73:300–1

© 2002 by The Society of Thoracic Surgeons 0003-4975/02/$22.00Published by Elsevier Science Inc PII S0003-4975(01)02850-8

hemorrhage suggesting infarction of a preexisting tumor(Fig 1).

A panel of endocrinology tests was performed: randomcortisol, 122 Nmol/L (normal 150–750); short synacthantest showed cortisol levels of 220 Nmol/L at 30 minutes(normal � 500): prolactin, 22 Mu/L (normal 150–500); freethyroxin, 8.8 Pmol/L (normal 9–24); thyroid stimulatinghormone, 0.16 Mu/L (normal 0.3–3.8); testosterone, 1.6Nmol/L (normal 10–30); follicle stimulating hormone,3.5 U/L (normal 0.8 –11.5); and lutenizing hormone,1.0 U/L (normal 0.8–12). On the basis of this pan-hypopituitary picture, he was started on a regimen ofsteroids and thyroid hormone replacement. Thereafter,his symptoms of malaise and nausea resolved.

Conservative management was subsequently em-ployed because the patient was clinically improving anddid not wish to undergo any further surgical interven-tion. He was discharged 22 days postop in good generalhealth, but with no sign of any resolution of his thirdnerve palsy. A repeat MRI 3 months postsurgery showedconsiderable shrinkage of the mass. On follow-up at 4months, he was found to be active, walking 3 miles a daywithout cardiac complaint. He was noted to have reducedfacial and body hair, and gynecomastia, which wastreated with testosterone patches. His left ptosis wasresolving and he had normal eye movement although heexperienced diplopia on upward gaze.

Comment

The mechanism of pituitary apoplexy is hemorrhage orinfarction. This may occur either spontaneously or fol-lowing various conditions such as anticoagulation, posi-tive pressure ventilation, radiotherapy, treatment withendocrinological trophic agents, prolonged coughing,

pregnancy after induction of ovulation with clomiphene,and trauma [1, 2]. Clinical manifestations can be neuro-logical: headache, lethargy, confusion, obtundation, uni-lateral, ptosis, meiosis, ophthalmoplegia involving cra-nial nerves 3, 4, and 6 (generally complete), visual fielddeficits, and hemiparesis. Endocrinological deficits arevariable: adrenal insufficiency with hypotension and syn-cope, hypothyroidism, and gonadotrophins deficiency.There have been several reports in the literature ofpituitary apoplexy after cardiac surgery [3–5]; most werein previously silent tumors such as the presented case.

Several factors in cardiac surgery have been implicatedincluding systemic anticoagulation, hypotension, posi-tive pressure ventilation, edema, hemodilution, reducedtissue oxygenation, and embolization [5].

Kovacs and Yao looked at the pituitaries of 33 patientswho had died within 10 days of major cardiac surgeryand found that 5 showed ischemic necrosis (15.2%). Themanagement of these cases has been controversial [3].Early surgery has been advocated in some series [4, 5] toprevent progression to a fatal state and to restore anyfunctional loss such as visual field defects. This has to bebalanced against the increased risk of morbidity or mor-tality for such an early (24 hours to 2 weeks) interventionafter major heart surgery.

In less severe presentations, such as ophthalmoplegiaor ptosis, surgery is not urgently indicated. Patients maybe closely monitored with regular computed tomo-graphic scans to await resolution of edema and hema-toma. However this must be tempered with the potentialfor incomplete recovery with intractable diplopia as adistressing sequel [6].

If neurosurgical intervention is indicated, the recom-mended approach to the pituitary is the trans-sphenoidalroute. The limited view of the surrounding structures(cavernous sinuses and carotid arteries) poses a risk ofbleeding which may be difficult to control, especially ifthe procedure is done early after cardiac surgery in thecontext of coagulopathy and abnormal platelet function[4]. For the reasons discussed above, a conservativeapproach was adopted in the presented case with agratifying clinical outcome.

References

1. Reid RK, Malachi EQ, Yen SSC. Pituitary apoplexy: a review.Arch Neurol 1985;42:712–9.

2. Rovit RL, Fein JM. Pituitary apoplexy: a review and reap-praisal. J Neurosurg 1972;37:280–5.

3. Kovacs K, Yao J. Pituitary necrosis following major heartsurgery. Z Cardiol 1975;64:52–7.

4. Savage EB, Gugino L, Starr PA, Black PM, Cohn LH, ArankiSF. Pituitary apoplexy following cardiopulmonary bypass:consideration for a staged cardiac and neurosurgical proce-dure. Eur J Cardiothorac Surg 1994;8:333–6.

5. Cooper DM, Bazaral MG, Furlan AJ, et al. Pituitary apoplexy:a complication of cardiac surgery. Ann Thorac Surg 1986;41:547–50.

6. Slavin ML, Budabin M. Pituitary apoplexy associated withcardiac surgery. Am J Ophthalmol 1984;98:291–6.

Fig 1. Magnetic resonance imaging of sagittal section through thepituitary fossa showing the mass (arrow) occupying the whole ofthe fossa.

301Ann Thorac Surg CASE REPORT ALZETANI ET AL2002;73:300–1 PITUITARY APOPLEXY POSTCARDIAC SURGERY