Fluid hydration in the form of IV fluid boluses should be given, with up to 2-3 L often required in the initial resuscitation stages to treat any concurrent dehydration. Afterwards, IV hydration with D5 NS can be beneficial, as it will help correct the hypoglycemia and hyponatremia often seen in these patients. Vasopressors can be started as needed, although these patients’ hypotension can be refractory to both fluids and vasopressors. Steroids are ultimately needed for vascular tone. The precipitating cause should be treated as indicated (1,2).
Corticosteroids have been used as drug treatment for some time. Lewis Sarett of Merck & Co. was the first to synthesize cortisone, using a complicated 36-step process that started with deoxycholic acid, which was extracted from ox bile .  The low efficiency of converting deoxycholic acid into cortisone led to a cost of US $200 per gram. Russell Marker , at Syntex , discovered a much cheaper and more convenient starting material, diosgenin from wild Mexican yams . His conversion of diosgenin into progesterone by a four-step process now known as Marker degradation was an important step in mass production of all steroidal hormones, including cortisone and chemicals used in hormonal contraception .  In 1952, . Peterson and . Murray of Upjohn developed a process that used Rhizopus mold to oxidize progesterone into a compound that was readily converted to cortisone.  The ability to cheaply synthesize large quantities of cortisone from the diosgenin in yams resulted in a rapid drop in price to US $6 per gram, falling to $ per gram by 1980. Percy Julian's research also aided progress in the field.  The exact nature of cortisone's anti-inflammatory action remained a mystery for years after, however, until the leukocyte adhesion cascade and the role of phospholipase A2 in the production of prostaglandins and leukotrienes was fully understood in the early 1980s.
While secondary or tertiary adrenal insufficiency (isolated glucocorticoid deficiency) does not lead to volume depletion, it decreases vascular tone, which leads to hypotension. Thus, adrenal crisis occurs less frequently in patients with secondary or tertiary adrenal insufficiency. When they do have adrenal crisis, it tends to be during acute stress, or with acute cortisol deficiency due to pituitary infarction or after surgical cure of Cushing's syndrome. (See "Clinical manifestations of adrenal insufficiency in adults", section on 'Secondary/tertiary adrenal insufficiency' .)