Acute adrenal insufficiency following unilateral radical nephrectomy: a case report

Geriatric Nephrology and Urology 8: 101–102, 1998. © 1998 Kluwer Academic Publishers. Printed in the Netherlands.

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Original article

Acute adrenal insufficiency following unilateral radical nephrectomy: A case report Michael H. Safir1 , Norm Smith1, Linda Hansen2 & James M. Kozlowski1 1 Department

of Urology and 2 Division of Endocrinology, Northwestern University Medical School, Chicago,

Illinois, USA Accepted 15 June 1998

Key words: adrenal insufficiency, renal cell carcinoma, surgical complications

Abstract Adrenal insufficiency following unilateral radical nephrectomy has not been previously described in medical literature. We present a 78-year-old male patient who experienced a difficult postoperative course with vague findings, and was ultimately diagnosed with acute adrenal insufficiency. Treatment with glucocorticoids and mineralocorticoids resulted in prompt control of the disease.

Since adrenal glands are paired, adrenal insufficiency rarely follows unilateral radical nephrectomy [1]. The signs and symptoms of postoperative adrenal insufficiency are vague and may mimic more common postoperative events. We present here a case of adrenal insufficiency following unilateral radical nephrectomy for renal cell carcinoma and review diagnosis and management algorithms.

Case report A 78-year-old male with stage T2b prostate cancer opted for neoadjuvant hormonal therapy followed by pelvic irradiation. He underwent radiographic staging including abdominopelvic CT which revealed a heterogeneous 5 cm left upper pole renal mass, without evidence of regional or metastatic disease. Examination of the abdomen was unremarkable. Blood chemistry and hemogram were within normal limits. The patient’s past medical history included hypertension and asthma. His medications on presentation included a calcium channel blocker and an angiotensin converting enzyme inhibitor. The patient underwent uneventful left radical nephrectomy. The first postoperative day, he became

agitated and converted to atrial fibrillation. He remained agitated and combative and became progressively disoriented, prompting a brain CT which was unrevealing for ischemia, bleed or tumor. Beginning the fourth postoperative day, he had a low-grade fever (100.5 ◦ F), anorexia, and serum sodium was noted to be 128 mg/dL. The patient was empirically given hydrocortisone 100 mg I.V., after which an early morning (5 a.m.) serum cortisol was drawn (= 3 mcg/dL). On evening rounds, the patient was noted to be alert and oriented to person, place, and time and remained afebrile. To establish a diagnosis of primary adrenocortical insufficiency, a cosyntropin stimulation test was performed, revealing low baseline cortisol = 2 mcg/dL and non-response to ACTH (cortisol = 2 mcg/dL). The patient was discharged to home two days later on oral glucocorticoids and fludrocortisone. Three days later, he presented to the emergency room complaining of lethargy and light-headedness. He was noted to be orthostatic and admitted that he had forgotten to take his medication. He was administered hydrocortisone 100 mg IV every eight hours (admitting serum cortisol