Silent Pituitary Infarction After Coronary Artery Bypass Grafting Procedure: Case Report and Review of Literature

Dany H. Zayour, MD; Sami T. Azar, MD


Endocr Pract. 2006;12(1):59-62. 

In This Article


The clinical and biochemical findings in this patient are consistent with anterior panhypopituitarism. The patient had no response of thyrotrophs or gonadotrophs to thyrotropin-releasing hormone or gonadotropin-releasing hormone stimulation tests, respectively. Although the insulin tolerance test is the "gold standard" for the diagnosis of secondary adrenal insufficiency, the minimal increase in the cortisol level to 6.6 µg/dL at 30 minutes and 9.6 µg/dL at 60 minutes in response to cosyntropin indicates adrenocortical atrophy as a result of chronic ACTH deficiency. We did not perform GH stimulation tests, but the very low IGF-I level in a patient with multiple pituitary hormone deficiencies is strong evidence of GH deficiency.[9] There were no posterior pituitary hormonal defects, as evidenced by the clinical absence of diabetes insipidus, although transient central diabetes insipidus has been reported after coronary artery bypass operation.[10] Because our patient had normal results of thyroid function tests a few months before the surgical procedure, the possibility of a previous defect in the pituitary-thyroid axis is excluded. One might argue that the elevated CK level was attributable to the statin therapy, which is notorious in causing this abnormality. The patient, however, had been taking simvastatin for 2 years and had a stable CK level at 260 U/L. Apart from the short episode of intraoperative hypotension with systolic blood pressure reaching 80 mm Hg and lasting about 30 minutes, the intraoperative and postoperative periods, as well as the time from the operation to presentation, were uneventful.

The patient had no symptoms or signs suggestive of pituitary apoplexy (mainly the absence of any acute neurologic or neuro-ophthalmologic defects). Such signs and symptoms usually indicate cranial nerve involvement in pituitary apoplexy, characterized by an acute hemorrhage into the pituitary gland. Moreover, the presence of an empty sella on MRI and the absence of symptoms until many months postoperatively indicate that the defect is that of silent pituitary infarction. It should be noted, however, that asymptomatic pituitary apoplexy has been reported previously.[11] Although the episode of intraoperative hypotension was brief, the only possible precipitating event for pituitary infarction is the coronary artery bypass grafting procedure. One might argue that this patient actually had a pituitary adenoma that spontaneously infarcted, as occasionally occurs. This possibility cannot be ruled out in our case as in previously reported cases because of the absence of a previous pituitary imaging study with normal findings. Nevertheless, the presence of a normal sellar size on MRI strongly argues against that point.

The literature includes 12 cases of pituitary apoplexy precipitated by a coronary artery bypass grafting procedure.[12,13,14,15,16,17,18,19,20] In all those cases, however, the presentation was that of pituitary hemorrhage with acute neuro-ophthalmologic defects and life-threatening endocrinologic deficits occurring within 48 hours postoperatively, and in 11 patients, surgical decompression was necessary. All 11 patients had evidence of pituitary adenomas, with 3 of them being diagnosed before the surgical procedure. Pathologic evidence of hemorrhage and necrosis was noted in these tumors. Furthermore, in an autopsy study published by Kovacs and Yao,[21] pituitary necrosis was present in 15% of the patients who died within 10 days after a coronary artery bypass procedure, an indication that this entity is probably underdiagnosed. Anticoagulant therapy is believed to be the underlying cause leading to pituitary hemorrhage and apoplexy.

Silent pituitary infarction after coronary artery bypass grafting has been reported previously in 3 male patients.[7,8] In the first patient, pituitary infarction was diagnosed 20 months after a coronary artery bypass operation, when he presented with impotence and signs of hypogonadism. Findings on endocrinologic evaluation were consistent with hypogonadotropic hypogonadism. Although the patient had already been receiving levothyroxine replacement therapy for primary hypothyroidism, dynamic pituitary testing revealed central hypoadrenalism and a lack of pituitary response to luteinizing hormone-releasing hormone stimulation. MRI of the pituitary confirmed pituitary infarction. The second patient presented 18 months postoperatively with malaise and, similar to the first patient, signs of hypogonadism. Dynamic testing and pituitary imaging also revealed pituitary infarction. In both of these patients, the presentation was delayed several months after the surgical procedure. An earlier sign of a metabolic defect was seen immediately postoperatively, however, with hyponatremia attributed to the syndrome of inappropriate antidiuretic hormone secretion in both cases. No episode of intraoperative hypotension was mentioned, but both patients had no precipitating event other than the surgical procedure.[7] In the third case, the authors reported an episode of hypotension complicating the operation and necessitating inotropic support. The presentation was again delayed to about 7 months postoperatively, with fatigue attributable to central hypothyroidism and hypogonadism as the presenting abnormality. MRI showed an empty sella with a small nonenhancing lesion, consistent with a pituitary adenoma. The patient had already been taking prednisolone for polymyalgia rheumatica.[8] It could be argued that the hypotension in this patient might not have been the cause of the pituitary infarction but was merely secondary to adrenal insufficiency caused by the pituitary tumor. Against this theory is the fact that the hypotension was reversed without the need for glucocorticoid therapy. Our patient survived the operation and the postoperative period with no corticosteroid therapy. All 3 patients in these previous reports, as well as our current patient, had no evidence of diabetes insipidus.

Our patient is the first reported case of silent hypopituitarism after a coronary artery bypass grafting procedure in a female patient. Furthermore, our patient was a postmenopausal woman. Hence, the presentation was that of hypothyroidism, not that of hypogonadism. To our knowledge, this is the first report of silent pituitary infarction manifesting as central hypothyroidism after a coronary artery bypass procedure. Silent pituitary infarction has been reported after other ischemic insults. Sheehan's syndrome[5] is a well-cited example of hypopituitarism occurring after childbirth, with distribution of symptoms and presentations over time similar to those features in our patient and the other 3 reported cases. This reflects the vulnerability of the pituitary circulation to vascular insults. Coronary artery bypass grafting is accompanied by major hemodynamic changes associated with the surgical procedure itself and with extracorporeal circulation, potentially leading to hypotension and nonpulsatile flow and causing infarction.