Adrenocortical insufficiency acute

Adrenocortical insufficiency Organ transplants Liver disease Adrenogenital syndrome Nephrotic syndrome Acute spinal cord injury Hyp ere alemia Hematologic disorders Myasthenia gravis Neoplastic disease... 

IV Diseases where high potassium levels may be encountered hyperkalemia renal failure and conditions in which potassium retention is present oliguria or azotemia anuria crush syndrome severe hemolytic reactions adrenocortical insufficiency (untreated Addison disease) adynamica episodica hereditaria acute dehydration heat cramps hyperkalemia from any cause early postoperative oliguria except during Gl drainage. 

In patients with longstanding hypothyroidism and those with ischemic heart disease, rapid correction of hypothyroidism may precipitate angina, cardiac arrhythmias, or other adverse effects. For these patients, replacement therapy should be started at low initial doses, followed by slow titration to full replacement as tolerated over several months. If hypothyroidism and some degree of adrenal insufficiency coexist, an appropriate adjustment of the corticosteroid replacement must be initiated prior to thyroid hormone replacement therapy. This prevents acute adrenocortical insufficiency that could otherwise arise from a thyroid hormone-induced increase in the metabolic clearance rate of adrenocortical hormones. 

Chronic adrenocortical insufficiency is characterized by weakness, fatigue, weight loss, hypotension, hyperpigmentation, and inability to maintain the blood glucose level during fasting. In such individuals, minor noxious, traumatic, or infectious stimuli may produce acute adrenal insufficiency with circulatory shock and even death. 

When acute adrenocortical insufficiency is suspected, treatment must be instituted immediately. Therapy consists of large amounts of parenteral hydrocortisone in addition to correction of fluid and electrolyte abnormalities and treatment of precipitating factors. 

Withdrawal symptoms disappear if the glucocorticoid is resumed, but as a rule they will in any case vanish spontaneously within a few days. More serious consequences can ensue, however, in certain types of cases and if adrenal cortical atrophy is severe. In patients treated with corticoids for the nephrotic syndrome and apparently cured, the syndrome is particularly likely to relapse on withdrawal of therapy if the adrenal cortex is atrophic (SEDA-3,305). In some cases, acute adrenocortical insufficiency after glucocorticoid treatment has actually proved fatal. It is advisable to withdraw long-term glucocorticoid therapy gradually so that the cortex has sufficient opportunity to recover. Table 5 lists methods of... 

The immediate management of patients with acute adrenal insufficiency includes intravenous therapy with isotonic sodium chloride solution supplemented with 5% glucose and corticosteroids and appropriate therapy for precipitating causes such as infection, trauma, or hemorrhage. Because cardiovascular function often is reduced in the setting of adrenocortical insufficiency, the patient should be monitored for evidence of volume overload such as pulmonary edema. After an initial intravenous bolus of 100 mg, hydrocortisone (cortisol) should be given by continuous infusion at a rate of 50-100 mg every 8 hours. At this dose, which approximates the maximum daily rate of cortisol secretion in response to stress, hydrocortisone overwhelms the 11/1HSD2 barrier in mineralo-corticoid-responsive tissues and has sufficient mineralocorticoid activity to meet all requirements. As the patient stabilizes, the hydrocortisone dose may be decreased to 25 mg every 6-8 hours. Thereafter, patients are treated in the same fashion as those with chronic adrenal insufficiency see below). 

For the treatment of suspected but unconfirmed acute adrenal insufficiency, 4 mg of dexam-ethasone sodium phosphate can be substituted for hydrocortisone, since dexamethasone does not cross-react in the cortisol assay and will not interfere with the measurement of cortisol (either basaUy or in response to the cosyntropin stimulation test). A failure to respond to cosyntropin in this setting is diagnostic of adrenal insufficiency. Often, plasma ACTH also is measured to provide information about the underlying etiology if the diagnosis of adrenocortical insufficiency is established. 

Use of OxyContin is associated with increased potential risks and it should be used only with caution in the following conditions acute alcoholism adrenocortical insufficiency (e.g. Addison s disease) CNS depression or coma delirium tremens debilitated patients kyphoscoliosis associated with respiratory depression myxedema or hypothyroidism prostatic hypertrophy or urethral stricture severe impairment of hepatic, pulmonary or renal function and toxic psychosis. 

These agents have use in diagnosis of adrenal disease and in controlling excessive production of corticosteroids, e.g. by corticotropin producing tumours of the pituitary (Cushing s syndrome) or by adrenocortical adenoma or carcinoma where the cause cannot be removed. They must be used with special care since they can precipitate acute adrenal insufficiency. Some members inhibit other steroid synthesis. 

Hypoth5n-oidism due to panhypopituitarism requires replacement with adrenocortical as well as with thyroid hormones. Use of levothyroxine alone can cause acute adrenal insufficiency. 

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