According to clinical practice guidelines, for newborns found to have bilateral inaccessible gonads, CAH evaluation should be considered. If virilizing CAH cannot be identified and treated, both boys and girls may undergo rapid postnatal growth and virilization. Nonclassic
In addition to the salt-wasting and simple-virilizing forms of CAH diagnosed in infancy,  a mild or "nonclassic" form exists, which is characterized by varying degrees of postnatal androgen excess, but is sometimes asymptomatic. The nonclassic form may be noticed in late childhood and may lead to accelerated growth, premature sexual maturation, acne, and secondary polycystic ovary syndrome. In adult males, early balding and infertility may suggest the diagnosis. The nonclassic form is characterized by mild subclinical impairment of cortisol synthesis; serum cortisol concentration is usually normal. Signs and symptoms
The symptoms of CAH vary depending upon the form of CAH and the sex of the patient. Symptoms can include:
Due to inadequate mineralocorticoids:
Vomiting due to salt-wasting, leading to dehydration and deathDue to excess androgens:

In extreme virilization, an elongated clitoris with a phallic-like structure is seen. Ambiguous genitalia, in some infants, occurs such that initially identifying  external genitalia as "male" or "female" is difficult. Early pubic hair and rapid growth occurs in childhood. Precocious puberty or failure of puberty to occur (sexual infantilism: absent or delayed puberty)
Excessive facial hair, virilization, and/or menstrual irregularity in adolescence
Infertility due to anovulation
Clitoromegaly, enlarged clitoris and shallow vaginaDue to insufficient androgens and estrogens:
Undervirilization in XY males can result in apparently female external genitalia.
Therefore, when cortisol is deficient, these processes (effectively) occur in the reverse direction. Although there are compensatory mechanisms that mitigate the impact of hypocortisolism, they are limited in their extent and the net effect is still hypoglycemia. Hyponatremia (due to hypoaldosteronism) - Aldosterone is the end product of the renin-angiotensin-aldosterone system that regulates blood pressure via blood pressure surveillance in the Kidney Juxtaglomerular apparatus. Aldosterone normally functions to increase sodium retention (which brings water as well) in exchange for potassium. Thus, lack of aldosterone causes hyperkalemia and hyponatremia. In fact, this is a distinguishing point from 11-hydroxylase deficiency, in which one of the increased products is 11-deoxycorticosterone that has weak mineralocorticoid activity. In 11-hydroxylase deficiency, 11-deoxycorticosterone is produced in such excess that it acts to retain sodium at the expense of potassium. It is this reason that patients with 11-hydroxylase deficiency do not show salt wasting (although sometimes they do in infancy), and instead have hypertension/water retention and sometimes hypokalemia. Hyperkalemia (due to hypoaldosteronism)
Elevated 17α-hydroxyprogesteroneClassic 21-hydroxylase deficiency typically causes 17α-hydroxyprogesterone blood levels >242 nmol/L. (For comparison, a full-term infant at three days of age should have <3 nmol/L. Many neonatal screening programs have specific reference ranges by weight and gestational age because high levels may be seen in premature infants without CAH.) Salt-wasting patients tend to have higher 17α-hydroxyprogesterone levels than non-salt-wasting patients. In mild cases, 17α-hydroxyprogesterone may not be elevated in a particular random blood sample, but it will rise during a corticotropin stimulation test.