On abdominal examination, the patient complained of slight peri-umbilical tenderness. Murphy's sign was negative and there was no costovertebral tenderness. Bowel sounds were easily heard. No herniae were present. A preoperative diagnosis of cholecystitis with cholelithiasis was made. LAB FINDINGS: Urinalysis-April 10-(random) 1. Specific Gravity-1.020 2. Pus cells-20- 25 per h .p.f. 3. RBC-1 - 3 per h.p.拢. 4. Sugar-acetone albumin-{) Urinalysis-April 14-(preoperative) Sugar-acetone-albumin-{) X-Ray-April 11 Cholecystogram showed a non-concentrating gall bladder containing at least one partially opaque calculus. Course in Hospital: On April 15, 1957, the patient underwent a cholecystectomy. Wangensteen suction was initiated early on first postoperative morning. The patient at this time was complaining of pain but seemed in satisfactory condition. When seen at noon of the same day he was in shock and died almost immediately, before steroid treatment could be commenced. Post Mortem Examination: The adrenals were reduced in size and on section showed a very thin pale (less than 1 mm.) yellowish grey cortex which totally lacked normal orange-yellow pigment. On exposure of the sella tursica in the brain, a cystic lesion was seen occupying the sella and enlarging it to thrice its normal size. The cyst compressed the optic nerves and indented the hypothalamus so only a thin rim of cerebral tissue remained over the third ventricle. No pituitary tissue was seen and the optic nerves appeared as flattened cords. On microscopic examination, the heart revealed congestion. The liver had a hamartoma and focal fatty infiltration. Chronic pyelonephritis was seen in the kidneys. There was loss of zonal architecture and lipoid in adrenal cortex but the medulla was normal. The pituitary showed neoplas-
MARcH, 1963
tic cells arranged in anastomosing columns supported by a fine reticular framework with areas of tumor necrosis and the mass was enclosed in a thin fibrous capsule. The tumor was described as a sinusoidal type chromophobe adenoma. Comment: The patient died of shock along with pulmonary edema along with acute congestion of the viscera due to a cholangitis complicating a recent cholecystectomy. The atrophy of the adrenal glands due to prolonged cortisone therapy was a definite contributing factor. This death could have been avoided had it been known that this patient had taken cortisone previously. DANGERS OF RAPID WITHDRAWAL OF CORTICOSTEROIDS When steroids are given to patients over prolonged periods and particularly in doses sometimes greatly exceeding the amount required for replacement therapy, several considerations arise. ( 1) Main Dangers These are potentially lethal because they are almost impossible to recognize. (a) Relative Hypoadrenocorticism, which involves: 1. atrophy of the adrenal cortex (except zona glomerulosa) 2. decrease in production of endogenous glucocorticoid hormones 3. suppression of the ability of the pituitary to secrete corticotrophin. Adrenal function may be restored within a few weeks of the acute withdrawal of exogenous steroid, but occasionally relative adrenal insufficiency may persist for from several to many months after the steroids have been stopped. Administration of cor路 ticotropin may speed return of adrenal function to normal but it may at the same time inhibit secretion of endogenous corticotropin. Cessation of therapy with corticotropin therefore removes the stimulus to adrenocortical secretion resulting in a temporary state of relative adrenal insufficiency. Although the essential mechanism is different than with adrenal steroids the end result is similar-i.e. hypoadrenalism.