Hydrocortisone adrenal insufficiency

The recent CORTICUS trial (hydrocortisone vs placebo) does not support the routine use of corticosteroids in the management of septic shock. No difference in 28-d mortality was observed between groups, regardless of baseline relative adrenal insufficiency. Duration of shock was shorter in the hydrocortisone group however, an increased incidence of hyperglycemia, sepsis, and recurrent septic shock was observed. This section reflects the 2004 consensus guidelines... 

Hydrocortisone 50 mg IV q6h or 100 mg IV q8h for 7 d in patients with septic shock requiring vasopressor support if relative adrenal insufficiency present... 

In patients presenting with acute adrenal crisis who have not been diagnosed previously with adrenal insufficiency, immediate treatment with injectable hydrocortisone and intravenous saline and dextrose solutions should be initiated prior to confirmation of the diagnosis because of the life-threatening nature of this condition. Determine and correct the underlying cause of the acute adrenal crisis (e.g., infection). 

Hydrocortisone for septic shock patients refractory to resuscitation and vasopressors, with adrenal insufficiency. 

Stress-induced adrenal insufficiency complicates 9% to 24% of septic patients and is associated with increased mortality. Adrenal-insuffident patients are identified by a adrenocorticotropic hormone (ACTH) stimulation test. Patients are given 250 meg ACTH and a cortisol level is checked within 30 to 60 minutes. Responders are defined as a greater than 9-mcg/dL increase in cortisol and non-responders as a less than 9-mcg/dL increase in cortisol. Septic shock patients refractory to resuscitation and vasopressors, and with adrenal insufifidency (non-responders to the ACTH test) should be administered intravenous hydrocortisone 200 to 300 mg per day in three divided doses for 7 days.24,44... 

Corticosteroids can be initiated in septic shock when adrenal insufficiency is present or when weaning of vasopressor therapy proves futile. A daily dose equivalent to 200 to 300 mg hydrocortisone should be continued for 7 days. Adverse events are few because of the short duration of therapy. 

Patients with adrenal insufficiency should carry a card or wear a bracelet or necklace that contains information about their condition. They should also have easy access to injectable hydrocortisone or glucocorticoid suppositories in case of an emergency or during times of physical stress, such as febrile illness or injury. 

Hydrocortisone is a relatively short-acting agent. For replacement therapy in adrenal insufficiency it is administered orally and in combination with fludrocortisone. Hydrocortisone sodium succinate is a water-soluble derivative which can be used parenter-ally in emergencies such as acute bronchospasm and hypersensitivity reactions like anaphylactic shock. 

Cortisone acetate and hydrocortisone are usually the corticoids of choice for replacement therapy in patients with primary adrenocortical insufficiency (such as Addison s disease), or after adrenalectomy where both glucocorticoid and mineralo-corticoid replacement is needed. In secondary adrenal insufficiency, associated with inadequate corticotrophin (ACTH) secretion, glucocorticoid replacement alone is usually adequate [62]. 

Synthetic glucocorticoids are prednisolone, prednisone, methylprednisolone, dexamethasone, betamethasone and triamcinolone (Table 13.2). Hydrocortisone is available as either succinate or phosphate salts for oral and intravenous administration. It is the drug of choice when a rapid effect is required, e.g. acute adrenal insufficiency, or as peri-operative replacement therapy. Prednisolone can also be given intravenously. It has about 0.8 of the mineralocorticoid activity of hydrocortisone. Prednisone is a prodrug that is converted to prednisolone in the body. For chronic therapy, synthetic steroids without mineralocorticoid activity are preferred, such as dexamethasone, betamethasone or triamcinalone. Beclo-metasone passes membranes poorly and is more active topically than when given orally. It is used as an aerosol for chronic rhinitis and asthma, and topically in severe eczema. Fludrocortisone is a synthetic halogenated derivate of cortisol that is used for its mineralocorticoid effect. 

Aminoglutethimide 250 mg orally twice daily and hydrocortisone 20 mg twice daily Fatigue, mild nausea Skin rash, adrenal insufficiency, myelosuppression... 

X-linked adrenoleukodystrophy (X-ALD) was suspected. Plasma was obtained for the measurement of very long chain fatty acids (VLCFA), which revealed a C26 0 concentration of 1.32 pg/mL, a C24 0/C22 0 ratio of 1.88, and a C26 0/C22 0 ratio of 0.08 (normal is < 0.02), confirming the biochemical diagnosis of X-ALD. Subsequent formal neuropsychological testing was obtained and revealed a performance IQ of 70. Adrenal function was assessed by corticotropin (ACTH) stimulation test and revealed adrenal insufficiency that was treated with replacement therapy with hydrocortisone. 

Prednisolone - The stress of surgery causes an increase in plasma adrenocorticotrophic hormone and cortisol concentrations. Cortisol secretion can rise from 30 mg/day to 50 mg/day following minor surgery and 150 mg/day following major surgery. However, an abrupt withdrawal after a prolonged period may lead to acute adrenal insufficiency, hypotension or shock. Thus it is important to continue SC s corticosteroid therapy and additional intravenous hydrocortisone may be administered peri-operatively. 

Because most adrenal crises occur because of glucocorticoid dose reductions or lack of stress-related dose adjustments, patients receiving corticosteroid-replacement therapy should add 5 to 10 mg hydrocortisone (or equivalent) to their normal daily regimen shortly before strenuous activities such as exercise. During times of severe physical stress (e.g., febrile illnesses, after accidents), patients should be instructed to double their daily dose until recovery. Treatment of secondary adrenal insufficiency is identical to primary disease treatment with the exception that mineralocorticoid replacement is usually not necessary. 

In 1948 cortisone was made from bile acids in quantity sufficient for clinical trial, and the dramatic demonstration of its power to induce remission of rheumatoid arthritis was published the following year. In 1950 it was realised that cortisone was biologically inert and that the active natural hormone is hydrocortisone (cortisol). Since then an embarrassingly large number of synthetic steroids has been made and offered to the clinician. They are derived from natural substances (chiefly plant sterols), the constitutions of which approach most nearly to that of the steroids themselves. A principal aim in research is to produce steroids with more selective action than hydrocortisone, which induces a greater variety of effects than desired in any patient who is not suffering from adrenal insufficiency. 

This occurs in hypopituitarism. In theory the best treatment is corticotropin, but the disadvantages of frequent injection are such that hydrocortisone is preferred. Usually less hydrocortisone is needed than in primary insufficiency. Special sodium-retaining hormone is seldom required, for the pituitary has little control over aldosterone production which responds principally to plasma potassium concentration and to the renin-angiotensin system. Thyroxine and sex hormones are given when appropriate. The general conduct of therapy does not differ significantly from that in primary adrenal insufficiency. 

In h)rpopituitarism there is a partial or complete deficiency of hormones secreted by the anterior lobe of the pituitary. The posterior lobe hormones (see below) may also be deficient in a few cases, e.g. when a tumour has destroyed the pituitary. Patients suffering from hypopituitarism may present in coma, in which case treatment is as for a severe acute adrenal insufficiency. Maintenance therapy is required, using hydrocortisone, th5Toxine, oestradiol and progesterone (in women) and testosterone (in men). For growth hormone see above. 

Prednisolone, USP. Prednisolone. J -hydrocortisone. Il/3.l7.2l-trihydroxypregna-l.4-diene-3.20-dione. has less salt-retention activity than hydrocortisone (see Table 23-8), but some patients have more frequently experienced complications such as gastric irritation and peptic ulcers. Because of low mineralocorticoid activity, it cannot be used alone fur adrenal insufficiency. Prednisolone is available in a variety of salts and esters to maximize its therapeutic utility (see Fig. 23-30) ... 

The corticosteroids have been the subject of much controversy in the management of septic patients. Corticosteroids suppress the activation of polymorphonuclear leukocytes, complement activation, release of TNF, and activation of the coagulation system involved in the cascades of sepsis. A recent study demonstrated a decrease in mortality (absolute reduction of 10%) with lower doses of hydrocortisone and fludrocortisone in patients with adrenal insufficiency requiring high-dose or increasing vasopressor therapy within the first 8 hours of septic shock. There was no benefit for those patients without adrenal insufficiency. In summary, routine use of corticosteroids in patients with sepsis or septic shock is not recommended until further study. 

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