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Ann Thorac Surg 1997;64:589-590
© 1997 The Society of Thoracic Surgeons

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Correspondence

Acute Adrenal Insufficiency After Coronary Artery Bypass Grafting

Department of Cardiothoracic Surgery, Shaare Zedek Medical Center, Po Box 3235, Jerusalem 91031 Israel

To the Editor:

We read with great interest the case report by Sutherland and Naik [1] regarding acute adrenal insufficiency after coronary bypass grafting. We would like to report a similar case that we experienced at our center after a coronary operation.

A 59-year-old man underwent elective coronary artery bypass grafting for unstable angina pectoris. His medical history was unremarkable. At operation, the left internal mammary artery was anastomosed to the left anterior descending artery and four saphenous vein grafts were anastomosed to the posterior descending, posterolateral, and obtuse marginal arteries. The aorta was cross-clamped for 65 minutes, and the patient received cold sanguineous antegrade intermittent cardioplegia. Total cardiopulmonary bypass time was 110 minutes, during which the patient's temperature drifted to 32°C and later rewarmed to 37°C. The operation was uneventful, and the patient was weaned from cardiopulmonary bypass without difficulty and without inotropic support. In the intensive care unit, inotropic support with norepinephrine was started due to hypotension with good cardiac output and low systemic vascular resistance. The patient was gradually weaned off the inotropic support and transferred to the ward for further postoperative care.

On the third postoperative day, a fever of 38.5°C, tachypnea, hypotension, and agitation developed. Blood, urine, and sputum cultures were taken and although the white blood cell count was normal, the patient was started on a regimen of broad-spectrum antibiotics because of the presumed diagnosis of sepsis. His condition continued to deteriorate and he was transferred back to the intensive care unit, where he was reintubated and mechanically ventilated. Multiorgan failure ensued with renal failure, malabsorption, and respiratory failure. An abdominal ultrasound did not show any abnormal findings. An abdominal computed tomographic scan showed a small cystic mass in the left adrenal gland. Urinary catecholamine levels were normal. There were no clinical signs of mineralocorticoid deficiency. All cultures were negative, and administration of antibiotics was stopped. Blood was sent for measurement of cortisol levels, and the patient was empirically started on intravenous hydrocortisone therapy with immediate dramatic improvement in his condition. He was weaned from all inotropic support within the next 24 hours. The blood cortisol levels were abnormally low, which confirmed our diagnosis of adrenal insufficiency. The patient continued to receive maintenance steroid therapy and was discharged from the hospital in good condition 20 days after the operation. Almost a year after the operation, the patient is still receiving a low dosage of maintenance steroids and is in good condition.

We agree with Sutherland and Naik that this diagnosis deserves a high level of suspicion in any patient whose postoperative course is unexpectedly poor, especially if the surgical procedure was uncomplicated. The clinical features of cortisol deficiency are diverse and not necessarily limited to the classic picture of mineralocorticoid deficiency with its biochemical profile.

Reference

1. Sutherland FWH, Naik SK. Acute renal insufficiency after coronary artery bypass grafting. Ann Thorac Surg 1996;62:1516–7.[Abstract/Free Full Text]

Cardiothoracic Unit, King's College Hospital, London SE5 9rs, United Kingdom

Reply To the Editor:

The similarity between our case and that of Fink and associates is striking. I feel sure that some such cases pass unrecognized and reiterate the high level of suspicion required for detection. In fact, detection and confirmation of frank adrenal insufficiency is so easy that I would go so far as to suggest that all cases of suspected sepsis be tested by random cortisol assay. Interestingly, sepsis itself may precipitate adrenal failure [1, 2], which is a further reason for testing these patients.

Since writing this article I have formed the opinion that there are a group of patients in whom a state of diminished adrenal responsiveness develops after operation but who cannot be classed as having frank adrenal failure. I have demonstrated this in 1 patient thus far and stress that existing diagnostic criteria are not sufficiently sensitive to detect this latter group of patients. This is one of my ongoing research interests.

References

1. Soni A, Pepper GM, Wyrwinski PM, et al. Adrenal insufficiency occurring during septic shock: incidence, outcome and relationship to peripheral cytokine levels. Am J Med 1995;98:266–71.[Medline]
2. Moran JL, Chapman MJ, O'Fathartaigh MS, et al. Hypocortisolaemia and adrenocortical responsiveness at the onset of septic shock. Intensive Care Med 1994;20:489–95.[Medline]

This Article Alert me when this article is cited Alert me if a correction is posted 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): Daniel Fink Shuli Silberman Fraser W. H. Sutherland Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Fink, D. Articles by Sutherland, F. W. H. Search for Related Content PubMed PubMed Citation Articles by Fink, D. Articles by Sutherland, F. W. H.