Acute Adrenal Insufficiency
This chapter defines the criteria for the diagnosis of adrenal insufficiency, its diagnosis, and the various modalities of treatment. Pitfalls in the diagnosis process are discussed, and the standards of practice are outlined.
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Acute Adrenal Insufficiency Lynn Loriaux
Précis 1. Clinical setting—Shock resistant to volume and presser resuscitation. 2. Diagnosis (a) History: Important complaints include weight loss, syncope, hypoglycemia, fatigue, and unexplained abdominal pain. Recent supraphysiological gluccoid treatment or a history of pituitary or hypothalamic disease including neurosurgery in the skull base and closed head trauma. Adrenal surgery, abdominal trauma, unexplained flank pain associated with anticoagulation, and the antiphospholipid antibody syndromes all increase the likelihood of primary adrenal failure. Medications that interfere with glucocorticoid synthesis, secretion, and action are obvious causes: ketoconzole, metyraprone, and mefipristone (RU-486). (b) Physical examination: Fever up to 104°, orthostatic hypotension, weight loss, hyperpigmentation of the skin, vitiligo, purpura, petechia, thrush, and calcification of the cartilage of the external ear are signs that can be associated with adrenal insufficiency. (c) Laboratory values: A total plasma cortisol of less than 20 μg/dL, hyponatremia, hypoglycemia, relative lymphocytosis, eosnophilia, pre-renal azotemia, and mild to moderate anion gap metabolic acidosis are common. (d) Imaging: Abnormalities of the hypothalamus and pituitary gland, and abnormalities of adrenal size. Bilaterally small adrenal glands can be the result of autoimmune adrenal destruction or adrenal suppression. Large adrenal glands are caused by infection, infarction, infiltration, and hemorrhage.
L. Loriaux, M.D., Ph.D. (*) Oregon Health and Science University, 3183 S.W. Sam Jackson Park Road, Portland, OR 97239, USA e-mail: [email protected] L. Loriaux (ed.), Endocrine Emergencies: Recognition and Treatment, Contemporary Endocrinology 74, DOI 10.1007/978-1-62703-697-9_1, © Springer Science+Business Media New York 2014
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3. Treatment—In addition to the standard treatment for shock, the treatment for acute adrenal insufficiency is intravenous replacement of hydrocortisone in a dose that replicates the plasma cortisol levels associated with critical illness. The standard dose is 50 mg hydrocortisone intravenously every 6 h until the crisis is past. If the pretreatment plasma cortisol is greater than 20 μg/dL, the cortisol administration can be discontinued when the crisis resolves. If the pretreatment cortisol level is less than 20 μg/dL, the intravenous dose of hydrocortisone should be reduced to an oral dose of 12–15 mg/m2/day until the diagnosis of adrenal insufficiency can be confirmed or excluded. It can require 12 h following the first dose of hydrocortisone before for the first glucocorticoid effects are clinically manifest. The most common untoward side effect of glucocorticoid therapy is failure to discontinue its administration when the crisis is past. Every attempt must be made to stop the administration of glucocorticoid at the earliest possible time to prevent the complications of iatrogenic Cushing’s syndrome which can quickly become the dominant clinical problem. A
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