CHAPTER 13 Endocrine Emergencies
I. GENERAL STRATEGY
A. Assessment
C. Planning and Implementation/Interventions
F. Age-Related Considerations
II. SPECIFIC ENDOCRINE EMERGENCIES
A. Adrenal Crisis
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.