Hyperaldosteronism: Difference between revisions
| (4 intermediate revisions by the same user not shown) | |||
| Line 6: | Line 6: | ||
* Secondary hyperaldosteronism – due to increased renin from conditions like renal artery stenosis, heart failure, or cirrhosis. | * Secondary hyperaldosteronism – due to increased renin from conditions like renal artery stenosis, heart failure, or cirrhosis. | ||
Primary hyperaldosteronism is an important and potentially reversible cause of secondary hypertension, accounting for 5–10% of hypertensive cases and up to 20% of treatment-resistant hypertension. It is often underdiagnosed in emergency settings. | Primary hyperaldosteronism is an important and potentially reversible cause of secondary hypertension, accounting for 5–10% of hypertensive cases and up to 20% of treatment-resistant hypertension. It is often underdiagnosed in emergency settings. <ref> Funder JW, Carey RM, Mantero F, et al. The management of primary aldosteronism: case detection, diagnosis, and treatment: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2016;101(5):1889–1916. doi:10.1210/jc.2015-4061 </ref> | ||
==Clinical Features== | ==Clinical Features== | ||
| Line 58: | Line 58: | ||
* Metabolic alkalosis | * Metabolic alkalosis | ||
Recommended ED labs: | Recommended ED labs: <ref> Young WF. Primary aldosteronism: renaissance of a syndrome. Clin Endocrinol (Oxf). 2007;66(5):607–618. doi:10.1111/j.1365-2265.2007.02775.x </ref> | ||
* Electrolytes (noting hypokalemia and alkalosis) | * Electrolytes (noting hypokalemia and alkalosis) | ||
| Line 88: | Line 88: | ||
==Disposition== | ==Disposition== | ||
Admit if: | |||
* Hypertensive emergency or end-organ damage | |||
* | |||
* Life-threatening hypokalemia or arrhythmia | |||
* | |||
* Severe electrolyte derangements | |||
Discharge with outpatient follow-up if: | |||
* Mild symptoms, stable vitals | |||
* | |||
* Newly discovered hypokalemia with controlled BP | |||
* | |||
* Reliable follow-up for endocrine evaluation | |||
==See Also== | ==See Also== | ||
[[Hypokalemia]] | |||
[[Hypertensive emergency|Hypertensive Emergency]] | |||
[[Pheochromocytoma]] | |||
[[Hypertension (main)|Renovascular Hypertension]] | |||
[[Cushing's syndrome|Cushing’s Syndrome]] | |||
==External Links== | ==External Links== | ||
[https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.120.15026 American Heart Association – Secondary Hypertension Guidelines] | |||
[https://www.ncbi.nlm.nih.gov/books/NBK539779/ NIH – Primary Aldosteronism Overview] | |||
==References== | ==References== | ||
<references/> | <references/> | ||
Latest revision as of 23:50, 5 May 2025
Background
Hyperaldosteronism refers to a condition of excess aldosterone secretion, typically leading to sodium retention, potassium excretion, and metabolic alkalosis. It is categorized into:
- Primary hyperaldosteronism (Conn syndrome) – autonomous overproduction of aldosterone, most commonly from an adrenal adenoma or bilateral adrenal hyperplasia.
- Secondary hyperaldosteronism – due to increased renin from conditions like renal artery stenosis, heart failure, or cirrhosis.
Primary hyperaldosteronism is an important and potentially reversible cause of secondary hypertension, accounting for 5–10% of hypertensive cases and up to 20% of treatment-resistant hypertension. It is often underdiagnosed in emergency settings. [1]
Clinical Features
- Hypertension (often severe or resistant)
- Hypokalemia, which may manifest as:
- Weakness
- Fatigue
- Muscle cramps
- Constipation
- Paresthesia
- Polyuria and polydipsia
- Metabolic alkalosis (less commonly symptomatic)
- Headache or nonspecific complaints
- Asymptomatic in some patients
Differential Diagnosis
- Essential hypertension
- Cushing’s syndrome
- Pheochromocytoma
- Renal artery stenosis
- Diuretic or laxative use
- Liddle syndrome
- Bartter/Gitelman syndromes
- Chronic licorice ingestion
Evaluation
Workup
Consider hyperaldosteronism in ED patients with:
- Severe or refractory hypertension
- Unexplained hypokalemia
- Metabolic alkalosis
Recommended ED labs: [2]
- Electrolytes (noting hypokalemia and alkalosis)
- Creatinine/BUN
- ECG (look for U waves, flattened T waves, arrhythmias)
- ABG or venous blood gas (if alkalosis suspected)
- Urine potassium (if available)
Diagnosis
Clinical suspicion in setting of hypertension + hypokalemia
Confirmatory outpatient testing with PAC/PRA ratio
Further endocrinology-guided evaluation determines surgical vs. medical management
Management
In the Emergency Department:
- Correct hypokalemia (PO or IV potassium)
- Avoid ACE inhibitors/ARBs until potassium is corrected
- Manage hypertension per usual protocols (IV meds if emergent)
- Initiate cardiac monitoring if K⁺ <3.0 mEq/L or if arrhythmia is present
Disposition
Admit if:
- Hypertensive emergency or end-organ damage
- Life-threatening hypokalemia or arrhythmia
- Severe electrolyte derangements
Discharge with outpatient follow-up if:
- Mild symptoms, stable vitals
- Newly discovered hypokalemia with controlled BP
- Reliable follow-up for endocrine evaluation
See Also
External Links
American Heart Association – Secondary Hypertension Guidelines
NIH – Primary Aldosteronism Overview
References
- ↑ Funder JW, Carey RM, Mantero F, et al. The management of primary aldosteronism: case detection, diagnosis, and treatment: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2016;101(5):1889–1916. doi:10.1210/jc.2015-4061
- ↑ Young WF. Primary aldosteronism: renaissance of a syndrome. Clin Endocrinol (Oxf). 2007;66(5):607–618. doi:10.1111/j.1365-2265.2007.02775.x