Abstract
Introduction:
Once diagnosed and localized, primary hyperaldosteronism responds extremely well to surgical excision. 1,2 Currently, laparoscopic adrenalectomy remains the gold standard for treating localized primary hyperaldosteronism. A successful excision requires an accurate diagnosis, proper localization, and meticulous dissection. This video depicts a left adrenalectomy that was removed for primary hyperaldosteronism.
Methods:
A 52-year-old female presented with a 20-year history of hypertension that required three antihypertensive medications. She underwent annual lab work and was found to be hypokalemic. She was referred to endocrinology for hypertension and hypokalemia. She underwent serum metanephrines and cortisol tests that were normal. Her plasma aldosterone/plasma renin ratio was only 12.6, but due to the suspicion of primary hyperaldosteronism, she underwent a 24-hour urine collection after salt loading. Her 24-hour urine aldosterone level was elevated at 14 micrograms, and she was started on spironolactone. An abdominal and pelvic CT scan did not show an adrenal lesion on either side. Based on the salt load test and clinical presentation with hypertension that required three medications and hypokalemia, the patient underwent an adrenal vein sampling. The AVS localized to the left gland with a ratio of 5 to 1. Based on this workup, the patient underwent a left laparoscopic adrenalectomy.
The patient was placed in a full right lateral decubitus position and flexed to open the lateral space. After obtaining abdominal access, the adrenalectomy began by mobilizing the spleen medially. The dissection was performed 1 cm from the splenic capsule to avoid any unnecessary bleeding. The superior aspect of the dissection extended to the left crus of the diaphragm. The patient’s anatomy required an extensive release of the splenic flexure, which was extremely cephalad. Blunt dissection was used for most of this part of the dissection.
The medial portion of the adrenal gland was incised towards the diaphragm. The adrenal gland was released from the splenic artery and pancreatic tail. Then, the lateral dissection of the gland was performed from the kidney. The inferior aspect of the gland was then dissected. Next, the adrenal vein was exposed and divided between clips. Finally, the remaining attachments of the lesion to the retroperitoneum were divided. Hemostasis was verified, and the specimen was placed in a bag and extracted.
Results:
Pathology showed adrenal cortical hyperplasia with a micronodule consistent with a clinical diagnosis of hyperaldosteronism. The patient was started on a clear liquid diet on postoperative day 1, and her potassium was 3.5. Her potassium supplements were discontinued.
She was advanced to a regular diet on postoperative day 2 and discharged home on the same day. Her blood pressure at discharge was 140/92, and her spironolactone was discontinued. At 6 months postoperatively, she remains off potassium and continues to take only one antihypertensive medication.
Conclusion:
Primary aldosteronism should be considered in patients with hypertension and hypokalemia. Proper workup is required to localize the biochemically appropriate gland. Laparoscopy remains the gold standard for patients that localize with primary hyperaldosteronism.
Patient Consent:
Authors have received and archived patient consent for video recording/publication in advance of video recording of the procedure.
Conflicts of interest:
There are no conflicts of interest.
Author Disclosure Statement:
There are no commercial associations during the last three years that might create a conflict of interest in connection with this video.
Runtime of video:
9 mins 9 secs.
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