Open access peer-reviewed chapter
Abstract
Primary hyperaldosteronism (PA) is the cause of endocrine hypertension, which commonly occurs in young patients with uncontrolled hypertension that leads to worsening cardiovascular-related mortality. Patients suspected of developing PA should have their plasma aldosterone concentration and plasma renin activity (PRA) assessed for screening purposes. After verifying the diagnosis of PA, adrenal venous sample (AVS) is the gold standard diagnostic technique for differentiating unilateral from bilateral disease. Since adrenalectomy may benefit patients with unilateral disease, laparoscopic adrenalectomy, a minimally invasive surgical approach that provides better postoperative outcomes than open surgery, has become the standard treatment for unilateral PA. Laparoscopic adrenalectomy resulted in a 53% cure rate of hypertension after surgery, as well as all patients had improved hypertension control, including the remission of hypokalemia. The conventional laparoscopic adrenalectomy approaches are transperitoneal and retroperitoneal, with similar postoperative outcomes. However, for general surgeons with limited laparoscopic adrenalectomy experience, the transperitoneal technique may offer an advantage over the retroperitoneal approach in terms of faster learning curve time, better surgical anatomy view, and the ability to resect adrenal tumors larger than 5 cm. This chapter focuses on the diagnosis and treatment of PA from the general surgeon’s perspective.
Keywords
- primary hyperaldosteronism
- hypertension
- adrenalectomy
- minimally invasive surgery
- transabdominal approach
1. Introduction
Primary hyperaldosteronism (PA) is a leading cause of endocrine hypertension attributable to the autonomous secretion of aldosterone by the adrenal gland, which inhibits the renin-angiotensin system, resulting in sodium retention, potassium diuresis, and volume overload. PA was reported as 5–11% patients with hypertension are related to 20% of drug-resistant hypertension [1, 2, 3]. In addition, patients may experience hypokalemia symptoms, such as proximal muscular weakness, muscle cramps, and palpitations. This chapter focused on the diagnosis process and the proper minimally invasive surgical treatment of PA from the general surgeon’s perspective.
2. Prevalence
The PA was classified into two subtypes, which are as follows: 1) unilateral adrenal gland involvement (adrenal adenoma) in 33–95% of patients, and 2) bilateral adrenal gland involvement (adrenal gland hyperplasia) in 5–60% of patients, according to certain studies. Thus, in patients with unilateral gland involvement, the goal of normalizing aldosterone levels by surgical management may be advantageous in contrast to the patients having bilateral adrenal involvement, these were more susceptible to medical treatment [4, 5].
Excessive aldosterone secretion may damage the cardiovascular system, increasing the risk of myocardial infarction, heart failure, cardiac arrhythmias (atrial fibrillation), stroke, renal function impairment, and consequences to increase cardiovascular-related mortality [6, 7].
The following were the indications for PA screening in hypertensive patients: 1) hypertension in young adults (age < 40 years), 2) severe/treatment-resistant hypertension (blood pressure > 160/100 mmHg), 3) sleep apnea, 4) hypokalemia, 5) atrial fibrillation without structural cardiac diseases, 6) first degree relative with PA, and 6) incidentaloma [8].
3. Screening test
3.1 Plasma aldosterone concentration and plasma renin activity
The plasma aldosterone concentration (PAC) is greater than 15 ng/dL, and the plasma renin activity (PRA) is less than 1 ng/mL/hour. This is the cut-off result for screening tests and was used to diagnose PA. Nonetheless, there are various methods for evaluating aldosterone levels in clinical settings, such as immunological assays and liquid chromatography-tandem MS/MS (LC–MS/MS), which may influence the cut-off values of each test.
As a result, aldosterone to renin ratio (ARR) greater than 30 ng/dL per ng/mL/h is more accepted in determining positive screening tests for PA with a sensitivity of 68–94%. To prevent a false negative result, antihypertensive medications, particularly angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB), should be discontinued between 4 and 6 weeks prior to the screening is recommended [9, 10].
4. Confirmatory test
Almost all patients who had positive screening test results needed a confirmation test to access dynamic aldosterone hypersecretion that affects the imbalance of the renin-angiotensin-aldosterone system to confirm the diagnosis of PA. However, the confirmation test may not be required in patients with the following conditions: 1) PAC levels larger than 20 ng/dL and 2) spontaneous hypokalemia.
4.1 Oral sodium loading test
After achieving good blood pressure control and collecting hypokalemia, the patients were required to intake 5000 milligrams (mg) of sodium (equal to 12.8 grams of sodium chloride) for 3 days. After 3 days of the high sodium diet, 24-hour urine samples were collected for sodium and aldosterone measurements. The diagnosis of PA was confirmed by: 1) 24-hour urinary sodium excretion greater than 200 mEq, and 2) 24-hour urinary aldosterone excretion greater than 12 micrograms. The sensitivity and specificity of the oral sodium loading test for the diagnosis of PA were reported as 96% and 93%, respectively [11, 12].
4.2 Intravenous saline infusion test
In order to reduce aldosterone production, this approach involves intravenous delivery of normal saline solution (0.9% sodium chloride) at a rate of 2 liters every 4 hours following an overnight fast. For PAC assessment, a blood sample was obtained after a complete saline infusion. In normal patients, the PAC level might be decreased to less than 5 ng/dL, however, a PAC level greater than 10 ng/dL is consistent with the diagnosis of PA with high sensitivity and specificity of 87% and 94%, respectively [13].
4.3 Fludrocortisone suppression test (FST)
Patients are given 0.1 mg of fludrocortisone orally every 6 hours for 4 days, along with potassium chloride and sodium chloride (6 gram/day) supplements to maintain serum potassium level greater than 4 mmol/L and 24-hour urine sodium excretion greater than 200 mEq. Blood samples were obtained at 7 AM to assess plasma cortisol, and at 10 AM to assess PAC, PRA, and cortisol levels. The diagnosis of PA was confirmed by: 1) a PAC level greater than 6 ng/dL, 2) a PRA level less than 1 ng/mL/h, and 3) a cortisol level at 10:00 AM that was lower than at 7:00 AM. In comparison with the saline infusion test, both tests were reliable, but FST seems to be more expensive and complex in the diagnosis of PA after a positive screening test [14].
4.4 Captopril challenge test
After 1 hour of the patients remaining in a sitting or standing position, captopril 25–50 mg was administered orally. Blood samples were taken to access PAC and PRA at 0, 1, and 2 hours after the medication was administered. The diagnosis of PA was confirmed by: 1) a decrease in PAC of more than 30% at 2 hours, 2) inability to suppress PAC to less than 11 ng/dL, and 3) an ARR of 20 ng/dL per ng/mL per hour. Furthermore, an ARR greater than 30 ng/dL per ng/mL per hour after ingesting captopril is strongly indicated for the diagnosis of PA [15, 16].
5. Radiologic imaging
5.1 Computed tomography scan (CT scan)
Contrast-enhanced CT scan is the first step in radiologic imaging in a PA patient for subtype evaluation, which is useful in distinguishing unilateral adrenal adenoma from bilateral adrenal hyperplasia, particularly in tumor sizes greater than 1–2 centimeters (cm). The CT scan detected unilateral adrenal involvement with 100% accuracy in a patient under the age of 35 with hypokalemia and a PAC greater than 30 ng/dL. The accuracy rate of CT scan declined in the patients over the age of 35, which is attributed to the high prevalence of bilateral disease and the limitations of the CT scan in differentiating the normal appearing adrenal gland from microadenomas (size less than 1 cm).
There are no CT criteria for differentiating adenoma from bilateral adrenal hyperplasia in terms of size and Hounsfield units. Nevertheless, the study by Lingam et al., demonstrates that an adrenal limb greater than 3 millimeters is beneficial in the diagnosis of adrenal hyperplasia with 100% sensitivity and specificity [17, 18]. Figure 1 illustrates CT scan-detected left aldosterone-producing adenoma.
Figure 1.
Computed tomography (CT) shows a well-defined left adrenal nodule (arrow) of size 1.3 cm. (18 HF on noncontrast CT) compatible with adrenal adenoma: (A) Sagittal view, and (B) coronal view.
5.2 Magnetic resonance imaging (MRI)
High-resolution MRI, including T1 and T2 weight images, has the same detection rate for unilateral adrenal adenoma as CT and should be used as a diagnostic adjunct in patients with strong clinical indications of PA and negative or equivocal CT findings. Furthermore, the diagnostic value of MRI for bilateral adrenal hyperplasia is limited in patients older than 40 years, with 68% sensitivity and 57% specificity [19, 20].
6. Role of lateralization with adrenal venous sampling (AVS)
Adrenal venous sampling is the gold standard diagnostic tool for differentiating unilateral from bilateral disease in PA patients. Aldosterone hypersecretion was discovered in the absence of an enlarged adrenal gland or a nodule. Thus, AVS improves the accuracy of the diagnosis of PA by 20–38% when compared to CT or MRI imaging, which can guide proper management and minimize unnecessary adrenalectomy in 20% of patients using the imaged-base technique.
The current guidelines for PA care are determined based on AVS findings. An interventional radiologist used percutaneous femoral vein access to perform this procedure. Blood samples were taken from the veins in the adrenal glands and the inferior vena cava (IVC).
The unilateral lateral disease was diagnosed when the ratio of normalized aldosterone to cortisol between the dominant and nondominant adrenal glands (lateralization index) was at least 4.0 and the ratio of aldosterone normalized to cortisol between the nondominant adrenal gland and peripheral blood (suppression ratio) was equal or less than 1.0.
Furthermore, AVS-based decision-making was found to be superior to image-based decision-making in unilateral pathology, resulting in hypokalemia correction and improved blood pressure control with 35–60% requiring no further antihypertensive drugs [21, 22, 23]. Figure 2 illustrates adrenal venous sampling in patients with left primary hyperaldosteronism.
Figure 2.
Angiographic imaging of adrenal venous sampling via the left adrenal vein.
7. Role of surgical management in primary hyperaldosteronism
Patients with bilateral disease were considered for medical treatment with mineralocorticoid receptor antagonists, such as spironolactone or eplerenone, in conjunction with potassium chloride supplementation. In contrast, surgical adrenalectomy may reduce aldosterone levels to normal in unilateral hyper-aldosterone-producing adenoma. Adrenalectomy can cure hypertension among 30–60% of patients and completely correct hypokalemia, resulting in a decreased incidence of atrial fibrillation and cardiovascular-related mortality in PA patients [24, 25].
7.1 Open surgery versus minimally invasive surgery
Historically, open adrenalectomy was the treatment of choice for functioning adrenal adenoma. After the development of minimally invasive surgical techniques, Gagner et al. first described laparoscopic adrenalectomy in 1992 for the management of Cushing’s syndrome and pheochromocytoma [26].
Laparoscopic adrenalectomy provides an advantage over open surgery in terms of decreased intraoperative blood loss, less postoperative complications, shorter return to diet time, shorter length of hospital stays, and faster return to normal activity [27].
Laparoscopic adrenalectomy is beneficial for long-term blood pressure control and correction of hypokalemia in patients with PA. The cure rate for hypertension was 51%, with conversion to open surgery and postoperative morbidity rates of 3.2% and 8.0%, respectively [28]. Currently, laparoscopic adrenalectomy is considered the standard treatment for unilateral aldosterone-producing adenoma.
7.2 Transperitoneal versus retroperitoneal approach
The transperitoneal and retroperitoneal approaches are used for standard laparoscopic adrenalectomy techniques. The retroperitoneal technique is advantageous in cases of previous extensive abdominal surgery to avoid visceral organ injury, but it should be avoided in adrenal tumors greater than 7 cm in size, since this may limit anatomical landmarks in the retroperitoneal space. Previous research indicates that both procedures are comparable in terms of operating time, intraoperative blood loss, hospital stay, and postoperative complications [29, 30].
Attributed to the reason that the author’s institution is a medium-sized university hospital, general surgeons must play an important role in the minimally invasive surgical management of patients with functional adrenal tumors, particularly pheochromocytoma and primary hyperaldosteronism.
Transperitoneal approach appears to be an appropriate surgical technique for general surgeons with limited experience in laparoscopic adrenalectomy because of 1) shorter learning curve time, 2) superior surgical view through the use of laparoscopy, 3) comfort with intraperitoneal anatomical landmarks over retroperitoneal space, and 4) ability to resect adrenal tumors larger than 5 cm. The retroperitoneal technique is appropriate for experienced surgeons who have conducted at least 20 procedures and also have a tumor size of less than 5 cm [31, 32].
8. Operative techniques for laparoscopic transperitoneal adrenalectomy
8.1 Right adrenalectomy
8.1.1 Patient position
The operation was performed under general anesthesia and the patients were placed in a left lateral decubitus position, and the surgical table was flexed between 100 and 120 degrees at an umbilical level to enhance the distance between the costal margin and the iliac crest [33, 34, 35, 36].
8.1.2 Trocars site placement
A 12 mm trocar was introduced into the peritoneal cavity using an open method at 3 cm below the right costal margin at the anterior axillary. Under laparoscopic guidance, two 5 mm working trocars were placed in the posterior axillary line and mid-clavicular line. The author preferred to add a 5 mm trocar at the subxiphoid for a fan-shaped liver retractor.
8.1.3 Operative technique
After carbon dioxide insufflation, pneumoperitoneum is created with a pressure of 10–12 mmHg. The triangular ligament was divided and the right lobe of the liver was lifted upward with a fan-shaped liver retractor. The posterior peritoneum was dissected with an electrocautery hook or harmonic scalpel (Ethicon Endo-Surgery INC - Johnson & Johnson, NJ, USA) to expose the right kidney, right adrenal gland, and inferior vena cava (IVC).
The first and most crucial step in right adrenalectomy is vascular control. Thus, the superomedial aspect of the adrenal gland, which is located between the confluence of the IVC and the right renal vein, was meticulously dissected to identify the right adrenal vein.
The right adrenal vein was clipped with nonabsorbable polymer clips (hem-o-lock(R), Teleflex Medical, Durham, NC, USA) and divided by a laparoscopic scissor or harmonic scalpel. The author recommended the use of double clips on the IVC site to avoid clip slippage, which could result in exsanguinate bleeding.
Following control of the right adrenal vein, the adrenal gland was raised up with an atraumatic grasper, and dissection should be extended to the posterior and lateral aspects to complete adrenal gland removal.
The gland is placed in a sterile bag before being retrieved via a 12 mm trocar incision that can be extended as needed. Before closing the skin incision, complete hemostasis was confirmed, and routine drainage was not recommended. Figure 3 illustrates the surgical technique for laparoscopic transperitoneal right adrenalectomy.
Figure 3.
Laparoscopic transperitoneal right adrenalectomy: (A) Position of the patient and placement of the trocars; (B) identification of the right adrenal vein; (C) clips control of the right adrenal vein; and (D) after removal of the right adrenal tumor.
8.2 Left adrenalectomy
8.2.1 Patient position
The patients were placed in the right lateral decubitus position and the operating table was flexed, as described in right adrenalectomy.
8.2.2 Trocars site placement
An open 12 mm trocar was introduced into the peritoneal cavity 3 cm below the left costal margin at the anterior axillary line. Two 5 mm and 12 mm working trocars were placed at the subxiphoid and mid-clavicular lines, respectively. An extra 5 mm trocar can be placed in the posterior axillary line as necessary for the fan-shaped retractor.
8.2.3 Operative technique
The procedure for creating pneumoperitoneum is the same as that described in right adrenalectomy. The splenic flexure colon and spleen were mobilized initially by dissecting the splenocolic, splenorenal, and lienorenal ligaments through the diaphragm for adequate exposure of the left adrenal gland.
The upper pole of Gerota’s fascia serves as a landmark for identifying the left adrenal gland during dissection. The dissection was carried out medially close to the level of the left renal vein. Meticulous dissection was required to locate the left adrenal vein, which was subsequently clipped and separated from the left renal vein using nonabsorbable polymer clips (hem-o-lock(R), Teleflex Medical, Durham, NC, USA).
The adrenal gland’s medial aspect was carefully dissected, and the small arterial branches from the aorta that supply the left adrenal gland were clipped and divided. Completer gland removal was accomplished by continuing dissection to the upper portion of the gland while avoiding harm to the splenic artery and pancreatic tail. After hemostasis was confirmed, the specimen was retrieved using a sterile bag. Figure 4 illustrates the surgical technique for laparoscopic transperitoneal left adrenalectomy.
Figure 4.
Laparoscopic transperitoneal left adrenalectomy: (A) Patient positioning and trocar site placement; (B) identification of the left adrenal vein; (C) control of the left adrenal vein with clips; and (D) control of the arterial supply to the left adrenal gland with clips.
8.3 Postoperative complication
For the right adrenalectomy, significant bleeding occurs as a result of IVC injury caused by avulsion or right adrenal vein or clip slippage, necessitating conversion to open surgery. This complication may have been avoided with proper trocar site placement and precise dissection to allow adequate exposure of the surgical landmarks via the laparoscopic view.
Left adrenalectomy complications included hollow viscus organ perforation, vascular injury, and pancreatic tail injury. These could be prevented by using the proper trocar site placement and surgical dissection technique. In the case of small adrenal tumors, the upper pole of Gerota’s fascia is an essential surgical landmark for determining the appropriate dissection plane to identify the adrenal gland. This technique could prevent the dissection of the incorrect plane, thereby preventing bleeding from the renal and splenic veins.
In the circumstance that renal artery or renal vein injury occurs during adrenal gland dissection. The damage site might be controlled with an atraumatic grasper and repaired with an intracorporeal suture. However, if the hemorrhage cannot be controlled, immediate conversion to open surgery will be required.
Hollow viscous organ perforation should be repaired with an intracorporal suture under laparoscopic vision, similar to pancreatic tail injury; in this circumstance, closed-suction drainage at the surgical site should be considered.
9. Postoperative disease monitoring
For immediate postoperative disease monitoring, blood tests for plasma aldosterone, renin, and potassium levels should start on the first day. Therefore, antihypertensive medications and potassium supplements should be discontinued or tapered to prevent interfering with biochemical measurements.
Furthermore, serum aldosterone and renin levels should be measured at 1 and 6 months after surgical management to confirm that PA is curable. Patients who underwent adrenalectomy under AVS-based therapy had a high biochemical cure rate of 80%, attributable to the improvement in hypertension control and hypokalemia cure rates [37, 38].
The postoperative hypertension cure rate following adrenalectomy was found to be 53% at 6 months and 49.6% at 12 months. Age older than 55 years, a long history of hypertension, and a tumor size greater than 2 cm are indeed risk factors for postoperative persistent hypertension. All of the patients, however, had curative hypokalemia and needed fewer antihypertensive medications following the surgery [39, 40, 41]. Figure 5 illustrates a surgical specimen from laparoscopic left adrenalectomy in PA patients.
Figure 5.
Surgical specimen: (A) Gross specimen reveals 1.5 and 0.3 cm of golden yellow adrenal adenoma, and (B) microscopic examination of tumor cells reveals an alveolar and trabecular pattern of growth without capsular or vascular invasion.
10. Conclusion
Laparoscopic adrenalectomy is the gold standard treatment for unilateral PA, with a low postoperative morbidity rate and an excellent clinical success rate for hypertension control. General surgeons, particularly in small to medium-sized hospitals, may play an important role in the surgical management of PA. Transperitoneal laparoscopic adrenalectomy is a safe and effective technique that is recommended for general surgeons with limited laparoscopic adrenalectomy experience.
Acknowledgments
The author wishes to thank Associate Professor Prinya Akkranurakul for the comments, who contributed in the preparation of this chapter.
Conflict of interest
The author declared no conflict of interest.
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