How is hyperaldosteronism coded in ICD-10? Does the etiology impact code choice?
Hyperaldosteronism occurs due to the excess production of aldosterone from the adrenal gland.
Hyperaldosteronism can initially present as essential and refractory hypertension and can often go undiagnosed. This disorder can be of primary or secondary origin, both presenting similarly but differentiated by a set of lab values and diagnostic studies. Treatment is specific to the individual causes of hyperaldosteronism.
Its primary or secondary origin can differentiate hyperaldosteronism.
Primary hyperaldosteronism is due to the excess production of the adrenal gland, more specifically the zona glomerulosa. This can present more commonly as a primary tumor in the gland known as Conn syndrome or bilateral hyperplasia. Rarer forms are unilateral adrenal hyperplasia, ectopic aldosterone-secreting tumors, aldosterone-producing adrenocortical carcinomas, and familial hyperaldosteronism type 1.
Secondary hyperaldosteronism occurs due to excess activation of the renin-angiotensin-aldosterone system (RAAS). This activation can take the form of a renin-producing tumor, renal artery stenosis, or edematous disorders like left ventricular heart failure, pregnancy, cor pulmonale, or cirrhosis with ascites.
▪ Primary hyperaldosteronism – E26.0 (HCC 23)
▪ Secondary hyperaldosteronism – E26.1 (HCC 23)
- Document the clinical findings which lead to the diagnosis of the primary condition responsible for the aldosteronism and the status, the diagnosis of secondary aldosteronism, and a plan of care.
- As with most secondary diagnoses due to an underlying primary condition, the causal condition should be identified and documented, if known.
▪ Secondary aldosteronism (E26.1) due to heart failure (I50.9)
▪ Alcoholic cirrhosis of liver with ascites (K70.31) and secondary hyperaldosteronism (E26.1)
▪ Aldosteronism, secondary (E26.1) due to severe renal artery stenosis (I70.1)
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