Endocrine Emergencies

CHAPTER 13 Endocrine Emergencies





I. GENERAL STRATEGY



A. Assessment




1. Primary and secondary assessment/resuscitation (see Chapter 1)


2. Focused assessment











3. Diagnostic procedures




























F. Age-Related Considerations




1. Pediatrics












2. Geriatrics


















II. SPECIFIC ENDOCRINE EMERGENCIES



A. Adrenal Crisis


Acute adrenal insufficiency or adrenal crisis occurs in response to an acute stressor, such as infections, hemorrhage, trauma, surgery, burns, pregnancy, or abrupt cessation of long-term steroid use. Adrenal insufficiency occurs when the adrenal cortex ceases to produce glucocorticoid and mineralocorticoid hormones. Primary causes of adrenal insufficiency may include autoimmune adrenalitis (Addison’s disease), tuberculosis, acquired immunodeficiency syndrome (AIDS), metastatic lung or breast cancer, and adrenal hemorrhage. Secondary causes of adrenal insufficiency may include sarcoidosis, pituitary tumor, chronic steroid use, pituitary stroke, and rarely, postpartum pituitary necrosis. Adrenal crisis should be suspected in patients who have hypotension unresponsive to fluid resuscitation and vasopressor medications. Death occurs because of circulatory collapse and hyperkalemia-induced dysrhythmia.




1. Assessment








2. Analysis: differential nursing diagnoses/collaborative problems




3. Planning and implementation/interventions






















4. Evaluation and ongoing monitoring (see Appendix B)









B. Diabetic Ketoacidosis


Diabetic ketoacidosis is a result of insulin deficiency and stress hormone excess. It typically occurs in insulin-dependent diabetes (type 1), but it may also occur in non–insulin-dependent diabetes (type 2). Lack of insulin causes decreased cellular glucose uptake, release of free fatty acids, and increased gluconeogenesis by the liver. Hyperglycemia promotes osmotic diuresis with dehydration, hyperosmolality, and electrolyte depletion. Counterregulatory (stress) hormones (glucagon, catecholamines, cortisol, and growth hormone) have anti-insulin effects and stimulate the release of free fatty acids. Free fatty acids are converted to ketone bodies, which release hydrogen ions, thereby contributing to metabolic ketoacidosis. Acidosis decreases myocardial contractility and cerebral function. Infection and stressful events are the usual precipitating factors, along with omission of insulin and new-onset diabetes. The goal of therapy is a gradual, even return to normal metabolic balance. Complications of therapy such as cerebral edema, hypoglycemia, and electrolyte imbalance may contribute to death during treatment.



Nov 8, 2016 | Posted by in NURSING | Comments Off on Endocrine Emergencies

Full access? Get Clinical Tree

Get Clinical Tree app for offline access