Bilateral Adrenalectomy

Glucocorticoid replacement - the moment the second gland is out this patient has no endogenous cortisol and never will again. Hydrocortisone is given around that point, with drug and timing from the endocrine team and who gives it agreed before incision.

Refractory hypotension after the second gland - this is adrenal insufficiency until proven otherwise: the vessels lose the permissive effect of cortisol on catecholamines and pressure stops answering normal pressor doses. Confirm the steroid was given, and give it if there is doubt, before escalating norepinephrine.

Cushing's habitus and the airway - central obesity, a fat pad over the upper back and a short thick neck make laryngoscopy and mask ventilation harder, so ramp for it and run the institutional difficult airway pathway, not a routine plan.

Buried veins - the same habitus hides peripheral access, so plan ultrasound-guided lines early rather than hunting for a vein after induction in a patient who may need pressor quickly.

Fragile skin, veins and bones - hypercortisolism thins the dermis, weakens capillaries and causes osteoporosis. Ordinary handling has fractured ribs and vertebrae in these patients. Use paper tape, hold pressure longer after venipuncture, and move the patient with lift sheets and enough hands that no limb is levered.

A two-part positioning problem - either prone for the posterior retroperitoneoscopic approach, with the face in a headrest and the tube inaccessible, or turned from one lateral position to the other partway through the case.

Every turn a fresh setup - reconfirm tube depth and bilateral breath sounds, check the eyes are free of pressure, re-level the arterial line, verify lines and catheter still run, and repeat the pressure-point check with the osteoporosis in mind.

Retroperitoneal insufflation - a stiff space held open at pressures above an abdominal laparoscopy, so venous return falls and cardiac output can drop in a way that mimics bleeding. Prone plus obesity also raises plateau pressures, so recruit and use PEEP.

Rising carbon dioxide - the retroperitoneum absorbs more than a transperitoneal case, so raise minute ventilation. If end-tidal keeps climbing despite that, feel for subcutaneous emphysema across the flank, back and chest before blaming the ventilator.

Glucose and potassium - cortisol excess causes insulin resistance and the intraoperative steroid pushes glucose higher, so check hourly and infuse rather than bolus. They also arrive hypokalemic and alkalotic, so correct potassium before induction.

Proximal myopathy and reserve - steroid myopathy wastes the shoulder and hip girdle and the accessory muscles, and these patients often cannot cough. Titrate blocking drug to a quantitative monitor, not to weight and confirm recovery before extubation.

The bilateral pheochromocytoma subset - alpha blockade beforehand and post-resection vasoplegia apply as in any pheochromocytoma, but two tumors means two catecholamine surges and two vein ligations, and the second collapse lands on a circulation depleted by the first. Do not wean vasopressor or volume after the first side.

Disposition and replacement - a monitored bed, continued glucocorticoid, mineralocorticoid started, serial glucose, and electrolytes followed for the shift from losing aldosterone. Extubate awake with the myopathy in mind, sitting up.

Handover in plain words - tell the receiving team this patient cannot make cortisol and never will, and that any hypotension overnight is adrenal insufficiency until proven otherwise rather than something to work up first.

Both adrenal glands come out in one operation for a short list of problems: adrenocorticotropic hormone (ACTH) dependent Cushing's syndrome that has failed pituitary surgery and medical therapy, bilateral pheochromocytoma in multiple endocrine neoplasia type 2 (MEN2) or von Hippel-Lindau (VHL) disease, and bilateral macronodular or micronodular adrenal hyperplasia. The operation is definitive because it removes the end organ rather than the drive. That is also its cost. Cortisol and aldosterone production stop the moment the second gland comes off, and the patient is adrenally insufficient for life. In ACTH-dependent disease, removing the feedback target leaves the pituitary corticotroph tumor unopposed and it can enlarge, which is Nelson's syndrome. Chronic hypercortisolism has already remodeled the patient on your table: central obesity, hypertension, hyperglycemia, hypokalemic alkalosis, osteoporosis, thin skin, and proximal myopathy.

Indication and workup - the biochemical diagnosis is settled long before the OR. For Cushing's, ACTH-dependent disease is confirmed and pituitary-directed treatment has already failed or is not possible; for MEN2 or VHL, genetic testing and metanephrines define bilateral pheochromocytoma; imaging maps both glands, their veins, and the relationship of the right gland to the inferior vena cava (IVC).

Approach selection - three routes are in use. Posterior retroperitoneoscopic adrenalectomy takes both glands with the patient prone and never enters the peritoneum. Lateral transperitoneal laparoscopy is the most familiar approach but only reaches one gland at a time, so the patient is turned and re-prepped halfway through. An anterior transperitoneal approach, laparoscopic or open through a midline or bilateral subcostal incision, reaches both glands with the patient supine and is chosen for large tumors, malignancy, or prior surgery that rules out the other routes.

Posterior retroperitoneoscopic technique - the patient is placed prone with the hips and knees flexed and bolsters under the chest and hips to let the abdomen hang free. Three ports go in below the 12th rib on each side and the retroperitoneal space is created with carbon dioxide at higher insufflation pressures than an abdominal case uses, because the retroperitoneum is a low-compliance space that has to be held open. Both sides are done through separate port sets without moving the patient.

Lateral transperitoneal technique - full lateral decubitus, operative side up on a beanbag, table flexed. The right gland is taken first because the right adrenal vein is short and drains straight into the IVC, so that side carries the higher chance of converting to open while the patient is still fresh. The patient is then rolled to the opposite lateral position, re-prepped, and redraped for the left.

Gland dissection - on each side the adrenal vein is identified and controlled early, with clips or a vascular stapler on the right. Arterial supply comes in as small branches from the inferior phrenic, aorta, and renal arteries and is divided with an energy device. The gland is freed from the upper pole of the kidney and surrounding fat.

Completeness matters - the surgeon aims to remove every fragment of cortical tissue. Any remnant left behind can hypertrophy under the sustained ACTH drive of Cushing's disease and cause biochemical recurrence, so the dissection is deliberately thorough on both sides.

Extraction and closure - each gland comes out in a retrieval bag through an enlarged port site. Fascia is closed at extraction sites, insufflation is released, and skin is closed. Open conversion is the fallback for bleeding, an adherent tumor, or a breached diaphragm.

Immediate handoff - the surgical and endocrine teams set the postoperative steroid taper and the mineralocorticoid start before the patient leaves the room, and the patient is scheduled for endocrine follow-up including surveillance for Nelson's syndrome after ACTH-dependent disease.

The permanent consequence starts in your OR. From the moment the second gland is out this patient depends on replacement glucocorticoid for life and on replacement mineralocorticoid, usually fludrocortisone, because the aldosterone-producing zona glomerulosa is gone with the rest of the cortex. Before they leave your care the plan for both should exist in writing, and before they leave the hospital they should have a steroid emergency card, an emergency injectable hydrocortisone kit, and sick-day rules. This is not floor nursing detail you can hand off and forget, because the failure it prevents, an adrenal crisis, presents as shock.

Every future anesthetic this patient has is a stress-dose case. Any subsequent surgery, sepsis, or trauma requires supplemental glucocorticoid because they cannot mount a cortisol response, and the history is easy to miss when the chart says only adrenalectomy. Ask directly about prior adrenal surgery in any patient with unexplained intraoperative hypotension who is on chronic steroid, and treat empirically rather than waiting for a cortisol level.