Hypoaldosteronism physical examination

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

Overview

Patients with hypoaldosteronism usually appear fatigued. Physical examination of patients with hypoaldosteronism is usually unremarkable, unless there is severe hyperkalemia. Increased level of serum potassium level may present with muscle tenderness, hyporeflexia/areflexia and cardiac arrhythmias. The physical exam may also represent findings of underlying condition such as chronic kidney disease or diabetic nephropathy.

Patients with hypoaldosteronism usually appear fatigued. Physical examination of patients with hypoaldosteronism is usually unremarkable, unless there is severe hyperkalemia. Increased level of serum potassium level may present with muscle tenderness, hyporeflexia/areflexia and cardiac arrhythmias. The physical exam may also represent findings of underlying condition such as chronic kidney disease or diabetic nephropathy.^[1]^[2]^[3]^[4]

If hypoaldosteronism is from Addison’s disease, changes in skin and hair may be observed such as:

Pigmented skin and mucous membranes – darkening (hyperpigmentation) of the skin, including areas not exposed to the sun; characteristic sites are skin creases (e.g. of the hands), nipples, and the inside of the cheek (buccal mucosa), also old scars may darken.
Absence of axillary and pubic hair in females as a result of loss of adrenal androgens.

Hyperkalemia can lead to:

Hyponatremia is unusual in isolated hypoaldosteronism since ADH is under inhibitory control of cortisol. However, in patients of Addison’s disease as a cause of hypoaldosteronism, there is decreased level of cortisol and aldosterone. Since there is no inhibition of ADH from cortisol, this leads to increased free water absorption and hyponatremia. Patients with hyponatremia may present with confusion when serum sodium level is <115 mmol/L.
Hyporeflexia/areflexia

↑ Sarkar SB, Sarkar S, Ghosh S, Bandyopadhyay S (2012). “Addison’s disease”. Contemp Clin Dent. 3 (4): 484–6. doi:10.4103/0976-237X.107450. PMC 3636818. PMID 23633816.
↑ Montague BT, Ouellette JR, Buller GK (2008). “Retrospective review of the frequency of ECG changes in hyperkalemia”. Clin J Am Soc Nephrol. 3 (2): 324–30. doi:10.2215/CJN.04611007. PMC 2390954. PMID 18235147.
↑ Diercks DB, Shumaik GM, Harrigan RA, Brady WJ, Chan TC (2004). “Electrocardiographic manifestations: electrolyte abnormalities”. J Emerg Med. 27 (2): 153–60. doi:10.1016/j.jemermed.2004.04.006. PMID 15261358.
↑ Humphreys M (2007). “Potassium disturbances and associated electrocardiogram changes”. Emerg Nurse. 15 (5): 28–34. doi:10.7748/en2007.09.15.5.28.c4252. PMID 17902552.