Intended learning outcomes
Describe the clinical presentation of primary hyperaldosteronism.
Discuss the preoperative optimisation strategies in patients with primary hyperaldosteronism.
Describe the expected postoperative clinical trajectory and management of patients with primary hyperaldosteronism.
Introduction
Primary hyperaldosteronism (PHA) is the most common cause of secondary hypertension, with a prevalence of 20% among patients with resistant hypertension [1–3]. Due to the occult nature of the condition, diagnosis is often delayed, and sometimes severe complications may be present at the time of the diagnosis [4]. It is not unusual for optimal management to be difficult, and prolonged attempts at treatment with multiple agents often yield only modest improvements. One of the main causes of PHA is an aldosterone-producing adenoma [3] for which, today, laparoscopic adrenalectomy is the preferred treatment option. The perioperative management of these patients poses a challenge to the perioperative physician. There is, however, significant scope for pre-operative optimisation, and every effort should be made to address modifiable aspects of the clinical condition to improve postoperative outcomes.
This case report illustrates some challenges encountered in the perioperative management of a patient with PHA and outlines strategies to improve postoperative outcomes.
Report
A 65-year-old man with a body mass index of 39 kg/m2 and a medical history of long-standing hypertension and type-2 diabetes mellitus (T2DM) was referred by his general practitioner to the endocrinology department due to resistant hypertension requiring four anti-hypertensive agents, including a calcium channel blocker, an angiotensin-converting enzyme inhibitor, a thiazide diuretic and an alpha channel blocker. Despite the quadruple anti-hypertensive therapy, the patient’s systolic blood pressure remained chronically elevated above 150 mmHg, with frequent readings of more than 180 mmHg. The patient was referred to our endocrinology team, who investigated his condition further. Laboratory investigations demonstrated a plasma aldosterone:renin ratio of 3100 (normal levels < 680), a serum aldosterone level of 620 pmol (reference range: 90–700 pmol), renin levels < 0.2 nmol/l/h (reference range: 0.5–3.5 nmol/l/h), and normal plasma metanephrine levels. A computed tomography (CT) scan demonstrated a 15-mm left adrenal nodule and a normal appearance of the contralateral adrenal gland. The findings, given the clinical context of resistant hypertension, were highly suggestive of PHA secondary to an aldosterone-producing adrenal adenoma; therefore, the patient was commenced on spironolactone, an aldosterone receptor antagonist. Following an Adrenal Multidisciplinary Team review, the decision was made to complete the investigations with adrenal venous sampling (AVS), which is considered the gold standard for distinguishing between unilateral adenoma and bilateral adrenal hyperplasia. The AVS showed a left-to-right ratio of 7:1, suggesting the left adrenal gland produced seven times more aldosterone than the right, confirming a diagnosis of a left aldosterone-producing adrenal adenoma.
The patient underwent laparoscopic left adrenalectomy with a planned admission to the Post Anaesthesia Care Unit (PACU) postoperatively.
The patient’s blood pressure prior to induction of anaesthesia was 210/92 mmHg. Anaesthetic induction was performed using propofol and remifentanil via target-controlled infusion. Remifentanil was titrated to maintain a target mean arterial pressure between 65 and 80 mmHg, requiring effect-site concentrations of 5–6 ng/ml. The intraoperative course was otherwise uneventful.
Postoperatively, the patient remained hypertensive, with systolic blood pressure persistently at approximately 200 mmHg, despite pain being well controlled and no other identifiable causes present. He required glyceryl trinitrate infusion in addition to the background five anti-hypertensive agents to achieve the target systolic blood pressure of 160–190 mmHg.
In addition to difficulties in blood pressure control, the patient complained of nausea and altered taste sensation, which negatively affected his oral intake. Over the subsequent 4 days, glyceryl trinitrate was gradually weaned off, nausea settled and oral intake improved. Blood pressure control was satisfactory on oral anti-hypertensive therapy, and the patient was stepped down to ward-based care, where he continued to make a good recovery.
On postoperative day 7, he was discharged to his home on five anti-hypertensive agents: amlodipine, bendroflumethiazide, doxazosin, losartan and spironolactone. Over the ensuing 4 months, his general practitioner weaned his anti-hypertensives down to three agents.
Similarly, his taste perception returned to normal after a few weeks following surgery.
Question to be answered
What is the anticipated response in postoperative blood pressure after adrenalectomy for PHA and are there any clinical predictors for that?
Discussion
PHA is an adrenal disorder resulting in excess aldosterone production, independent of any physiological stimulus and of its major regulator, the renin–angiotensin–aldosterone system [4]. Currently, it is the most common cause of secondary hypertension with a 10% prevalence in hypertensive patients and up to 20% amongst those with resistant hypertension [1, 3]. Aldosterone is the main mineralocorticoid hormone secreted by the adrenal cortex [5]. Its primary function is to increase sodium reabsorption with the subsequent water reuptake, therefore maintaining normal blood pressure [6]. It also increases potassium secretion by renal tubular cells [5]. Accordingly, excessive aldosterone levels lead to sodium retention, volume expansion, elevated blood pressure, and hypokalaemia. Compared with patients with essential hypertension, matched by age and blood pressure, patients with PHA have an increased cardiovascular risk [7], with a higher prevalence of myocardial infarction and stroke [5, 8]. This prevalence is thought to be due to the proinflammatory and profibrotic effects of aldosterone on the cardiovascular system [9].
Aldosterone also exerts extra-renal effects via receptors in the colon, regulating local salt and water homeostasis, and via central receptors, presumably including those within the taste buds, modulating sodium ingestion [10].
There are various subtypes of PHA. The two most common are bilateral idiopathic hyperaldosteronism (IHA) and aldosterone-producing adenoma (APA). The former represents 60% of the cases, while the latter 35% [2, 7].
The clinical presentation is nonspecific. Patients usually present with severe hypertension, metabolic alkalosis and occasionally signs and symptoms of hypokalaemia. The latter, when present, can cause a variety of neuromuscular manifestations, including paraesthesia, visual disturbances, and occasionally tetany [2].
Patients suffering from PHA tend to have variable degrees of renal impairment, which may be masked by glomerular hyperfiltration associated with the aldosterone escape effect. This occurs because excess aldosterone elevates the blood pressure, inducing pressure natriuresis, pressure diuresis and the formation of natriuretic peptides. All these factors combined lead to increased diuresis and natriuresis, opposing the water-retention and sodium-retention effects of aldosterone [5]. Due to these mechanisms, patients with PHA do not tend to present with severe volume overload [11].
The diagnostic approach involves confirming high aldosterone and suppressed renin activity levels followed by subtype determination with a CT scan and an adrenal venous sample, to determine the treatment required [4, 11].
Treatment of PHA aims to either normalise circulating aldosterone levels or block mineralocorticoid receptors (MR), thereby improving blood pressure control and potassium levels. In unilateral cases, the treatment of choice is surgical, with laparoscopic adrenalectomy being the gold standard [1]. In bilateral causes, MR antagonist therapy is the preferred option.
Anaesthetic management
Thorough preoperative evaluation is essential, with particular attention to any pre-existing co-morbidities such as cardiovascular disease, renal dysfunction and cerebrovascular disease. Optimisation of blood pressure and potassium levels is of particular importance to ensure stability on the day of the surgery.
This is mainly achieved with MR antagonists, such as spironolactone, which should be administered in small doses, with the dose increased gradually to its maximum, if necessary. In patients in whom hypokalaemia persists, despite MR antagonists, potassium supplements may be prescribed.
Anaesthetic management will be strongly influenced by the degree of physiological optimisation achieved preoperatively.
The level of monitoring is tailored to individual patients but, in cases of adequate pre-optimisation, invasive monitoring is usually not necessary [12].
The anaesthetist needs to be prepared for haemodynamic changes, particularly during the manipulation of the adrenal gland during dissection and resection, which may lead to catecholamine release from the adrenal medulla, although this is usually not as severe during resectioning of phaeochromocytoma [13]. Glucocorticoid supplementation is not routinely indicated [8].
Postoperative management
Vigilance in the postoperative period is paramount, with increased attention to aldosterone and potassium levels and to the development of complications, such as hypotension, impaired renal function and hyperkalaemia [3]. Serum aldosterone levels should be checked on postoperative day 1.
Renal impairment is likely to manifest during the initial postoperative days as the masking effect of aldosterone recedes. After laparoscopic adrenalectomy, the true kidney function becomes apparent.
Hyperkalaemia is a possible early complication, as the contralateral zona glomerulosa is often completely suppressed. Approximately 16% of patients with unilateral APA develop postoperative hyperkalaemia following resection. One predictor of postoperative hyperkalaemia is preoperative renal dysfunction [1]. Therefore, electrolytes and renal function should be followed up closely after surgery, monitoring potassium levels and creatinine weekly for 4 weeks [3, 7].
Regarding blood pressure, hypertension will be cured or improved between 1 and 6 months after surgery. The former occurs in 30–40% of patients, while the latter occurs in approximately 90% of patients [1]. Studies have identified factors that predict hypertension cure after surgery, including younger age, female sex, shorter duration of hypertension, fewer anti-hypertensive drugs (fewer than two), lack of a family history of hypertension, lower body mass index, higher preoperative ratio of plasma aldosterone concentration to plasma renin activity, and higher urine aldosterone levels [1, 3, 14]. Also, persistent hypertension may be due to underlying primary hypertension or to the development of nephrosclerosis after many years of poorly controlled hypertension [15].
Lastly, regarding patients’ altered taste perception, studies have shown that impaired sodium chloride taste perception occurs in PHA. This altered taste perception tends to improve following both medical and surgical treatment for PHA [10]. Table 1 summarizes the clinical considerations that anesthesiologists need to have with PHA patients throughout the perioperative period.
Table 1 Anaesthetic consideration for the management of patients with PHA
| Preoperative | Intraoperative | Postoperative |
| Optimise blood pressure (goal < 160/100 mmHg) | Expect haemodynamic changes | Measure aldosterone levels on day 1 after surgery. And then once in the 3 months after surgery and once again in the year following the surgery |
| Screen for cardiovascular and cerebrovascular disease | Glucocorticoid supplementation usually not required | Monitor serum potassium levels daily on the first days after surgery and then weekly for 4 weeks |
| Screen for renal disease | Invasive monitoring tailored to specific patient needs (e.g. co-morbidities) | Monitor renal function closely for at least 4 weeks |
| Monitor and correct hypokalaemia | Monitor blood pressure and downtitrate anti-hypertensive therapy as necessary | |
| Start MR antagonist (e.g. spironolactone, eplerenone) | Long-term follow-up (6 months) of blood pressure | |
| Start potassium supplements if required |
This case illustrates a classic presentation of PHA. The patient had been referred to the department with a long history of poorly controlled hypertension, which was not optimised preoperatively, as evidenced by his preoperative blood pressure. It is not rare for hypertension to persist postoperatively, despite its underlying cause having been surgically removed. One theory for this is that secondary hypertension masks co-existing primary hypertension [13]. The patient did not have any of the favourable factors for hypertension resolution, namely, he was male, had a high BMI, a long history of hypertension, and he required treatment with up to five anti-hypertensive agents. His only positive predictor for the resolution of the hypertension was a high aldosterone: plasma renin activity ratio. His blood pressure had only begun to improve at approximately 4 months after surgery, which allowed slow weaning off the anti-hypertensive agents.
In conclusion, given the risks of poorly controlled hypertension and electrolyte imbalance during the perioperative period, it is paramount for the perioperative physician to have a thorough understanding of the nature of PHA, to provide adequate management during the pre-, intra- and postoperative periods. It is also crucial to have an honest discussion with the patient and manage their expectations regarding the effect of the surgery on blood pressure control.
Declarations and conflicts of interest
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Not applicable to this article.
Patient consent
The author declares that the patient has provided written informed consent to the author for publication, secured in accordance with the journal’s patient consent policy before publication.
Conflict of interest statement
The author declares no conflicts of interest with this article.
Artificial intelligence declaration
Artificial intelligence tools were used solely for language polishing. All clinical content, interpretation, references and final revisions were undertaken independently and verified by the author.
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