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ESSENTIALS OF DIAGNOSIS
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Weakness, abdominal pain, fever, confusion, nausea, vomiting, and diarrhea Low blood pressure, dehydration; skin pigmentation may be increased Serum potassium high, sodium low, BUN high Cosyntropin (ACTH1 24) unable to stimulate a normal increase in serum cortisol
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Acute adrenal insufficiency is an emergency caused by insufficient cortisol Crisis may occur in the course of treatment of
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other conditions (eg, hypothyroidism, diuretic use, heart failure, cirrhosis, vomiting, diarrhea, severe illness, or major surgery) Acute adrenal insufficiency must be distinguished from an acute abdomen in which neutrophilia is the rule, whereas adrenal insufficiency is characterized by a relative lymphocytosis and eosinophilia More than 90% of serum cortisol is protein bound and low serum levels of binding proteins result in misleadingly low serum cortisol determinations by most assays Nearly 40% of critically ill patients, with serum albumin < 25 g/dL, have low serum total cortisol levels but normal serum free cortisol levels and normal adrenal function
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chronic insufficiency, or it may be the presenting manifestation of adrenal insufficiency Acute adrenal crisis is more commonly seen in primary adrenal insufficiency (Addison s disease) than in disorders of the pituitary gland causing secondary adrenocortical hypofunction Adrenal crisis may occur in the following situations: (1) following stress, eg, trauma, surgery, infection, or prolonged fasting in a patient with latent insufficiency; (2) following sudden withdrawal of adrenocortical hormone in a patient with chronic insufficiency or in a patient with temporary insufficiency due to suppression by exogenous corticosteroids or megestrol; (3) following bilateral adrenalectomy or removal of a functioning adrenal tumor that had suppressed the other adrenal; (4) following sudden destruction of the pituitary gland (pituitary necrosis), or when thyroid hormone is given to a patient with hypoadrenalism; and (5) following injury to both adrenals by trauma, hemorrhage, anticoagulant therapy, thrombosis, infection or, rarely, metastatic carcinoma
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If the diagnosis is suspected, draw a blood sample for cortisol determination and treat with hydrocortisone, 100 300 mg intravenously, and saline immediately, without waiting for the results Thereafter, give hydrocortisone phosphate or hydrocortisone sodium succinate, 100 mg intravenously immediately, and continue intravenous infusions of 50 100 mg every 6 hours for the first day Give the same amount every 8 hours on the second day and then adjust the dosage in view of the clinical picture Since bacterial infection frequently precipitates acute adrenal crisis, broad-spectrum antibiotics should be administered empirically while waiting for the results of initial cultures Hypoglycemia should be vigorously treated while serum electrolytes, BUN, and creatinine are monitored
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Clinical Findings
A Symptoms and Signs
The patient complains of headache, lassitude, nausea and vomiting, abdominal pain, and often diarrhea Confusion or coma may be present Fever may be 406 C or more The blood pressure is low Recurrent hypoglycemia and reduced insulin requirements may present in patients with preexisting type 1 diabetes mellitus Other signs may include cyanosis, dehydration, skin hyperpigmentation, and sparse axillary hair (if hypogonadism is also present) Meningococcemia may be associated with purpura and adrenal insufficiency secondary to adrenal infarction (Waterhouse Friderichsen syndrome)
B Convalescent Phase
When the patient is able to take food by mouth, give oral hydrocortisone, 10 20 mg every 6 hours, and reduce dosage to maintenance levels as needed Most patients ultimately require hydrocortisone twice daily (am, 10 20 mg; pm, 5 10 mg) Mineralocorticoid therapy is not needed when large amounts of hydrocortisone are being given, but as the dose is reduced it is usually necessary to add fludrocortisone acetate, 005 02 mg daily Some patients never require fludrocortisone or become edematous at doses of more than 005 mg once or twice weekly Once the crisis has passed, the patient must be evaluated to assess the degree of permanent adrenal insufficiency and to establish the cause if possible
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