Pathophysiology of hyponatremia after transsphenoidal pituitary surgery.

Hyponatremia after pituitary surgery is presumed to be due to antidiuresis; however, detailed prospective investigations of water balance that would define its pathophysiology and true incidence have not been established. In this prospective study, the authors documented water balance in patients for 10 days after surgery, monitored any sodium dysregulation, further characterized the pathophysiology of hyponatremia, and correlated the degree of intraoperative stalk and posterior pituitary damage with water balance dysfunction. Ninety-two patients who underwent transsphenoidal pituitary surgery were studied. To evaluate posterior pituitary damage, a questionnaire was completed immediately after surgery in 61 patients. To examine the osmotic regulation of vasopressin secretion in normonatremic patients, water loads were administered 7 days after surgery. Patients were categorized on the basis of postoperative plasma sodium patterns. After pituitary surgery, 25% of the patients developed spontaneous isolated hyponatremia (Day 7 +/- 0.4). Twenty percent of the patients developed diabetes insipidus and 46% remained normonatremic. Plasma arginine vasopressin (AVP) was not suppressed in hyponatremic patients during hypoosmolality or in two-thirds of the normonatremic patients after water-load testing. Only one-third of the normonatremic patients excreted the water load and suppressed AVP normally. Hyponatremic patients were more natriuretic, had lower dietary sodium intake, and had similar fluid intake and cortisol and atrial natriuretic peptide (ANP) levels compared with normonatremic patients. Normnonatremia, hyponatremia, and diabetes insipidus were associated with increasing degrees of surgical manipulation of the posterior lobe and pituitary stalk during surgery. The pathophysiology of hyponatremia after transsphenoidal surgery is complex. It is initiated by pituitary damage that produces AVP secretion and dysfunctional osmoregulation in most surgically treated patients. Additional events that act together to promote the clinical expression of hyponatremia include nonatrial natriuretic peptide-related excess natriuresis, inappropriately normal fluid intake and thirst, as well as low dietary sodium intake. Patients should be monitored closely for plasma sodium, plentiful dietary sodium replacement, mild fluid restriction, and attention to symptoms of hyponatremia during the first 2 weeks after transsphenoidal surgery.

Diseases of the adrenal gland.

The reader should have a better working knowledge of several rare adrenal diseases after reading this article. Although they are rare, these adrenal diseases may be seen in many nursing settings. Astute nursing assessment and monitoring of signs and symptoms of these diseases are essential during diagnosis and treatment. A detailed case study illustrates Cushing's syndrome and pheochromocytoma as well as adrenal insufficiency.

Isolated hyponatremia after transsphenoidal pituitary surgery.

A retrospective analysis was performed to study the fluid and sodium status of patients undergoing transsphenoidal surgery (TS) for Cushing's disease. We evaluated the time of onset, duration, and relative incidence of isolated hyponatremia and identified possible factors associated with it. Of 58 patients that underwent TS over 1 yr, 52 without postoperative diabetes insipidus or volume depletion were studied. Isolated hyponatremia after TS for Cushing's disease occurred in 21%, and symptomatic hyponatremia (plasma sodium, < or = 125 mmol/L) with new onset headache, nausea, and emesis occurred in 7.0% of all operated. These later patients escaped monitoring and intervention for 24 h. The development of hyponatremia began early in the postoperative period and progressed slowly over 7 days. Maximum antidiuresis occurred on postoperative day 7. Vasopressin levels measured in two patients while hypoosmolar suggested that unregulated vasopressin release contributed to the hyponatremia. Cortisol levels, glucocorticoid replacement, and pituitary adenoma size were similar in normonatremic and hyponatremic patients. Patients combining a history of an estrogenic milieu and documented posterior pituitary trauma at surgery experienced lower nadir plasma sodium. All hyponatremic patients were fluid restricted, and none developed progressive neurological symptoms, morbidity, or mortality. We speculate that the mild degree and slow rate of development of hyponatremia and/or active monitoring and intervention contributed to the good outcome.

Adrenocortical insufficiency: a medical emergency.

Adrenal insufficiency is a deceptive disorder. Insidious in onset, chronic in nature, it can suddenly progress into an acute life-threatening condition that may mimic disorders of vastly different etiologies. The result can be a lethal delay in diagnosis. Prompt diagnosis and replacement of glucocorticoids and fluids are essential for survival. Acute adrenal insufficiency is frequently an exacerbation of an underlying chronic disorder of the adrenal cortex or pituitary gland. Yet any patient who has been treated with suppressive doses of glucocorticoids (e.g., cortisol, prednisone), experienced overwhelming sepsis, has received anticoagulant therapy, or has endstage metastatic carcinoma may suddenly develop adrenal insufficiency along with its deadly sequela of hypovolemic shock, hyperkalemia, hyponatremia, and hypoglycemia. Successful management of this condition requires not only a heightened clinical awareness of adrenal insufficiency, but effective stress reduction interventions and a thorough patient and family teaching program to support lifelong control of the disease.

Endocrinopathies of hyperfunction: Cushing's syndrome and aldosteronism.

Increased function of the adrenal cortex is a normal response in times of physiologic and psychologic stress. Adrenal cortical secretions (e.g., glucocorticoids, aldosterone) orchestrate a multitude of internal processes aimed at maintaining homeostasis and psychologic integrity. Many patients admitted to a critical care unit will manifest some increase, even minor, in adrenal function. However, excessive secretions of these hormones can have a lethal effect of fluid and electrolyte balance, energy metabolism, and immune function. Cushing's syndrome denotes a disorder characterized by increased circulating levels of glucocorticoids (primarily cortisol). An easily recognizable disorder, it may arise from pathology of the adrenal cortex or the anterior pituitary glands, ectopic secretions from a nonendocrine tumor, or from excessive doses of exogenously administered glucocorticoids. Cushing's syndrome is rarely an admitting diagnosis to critical care but is a disorder that can seriously affect recovery from coexisting illnesses if not treated. Aldosteronism, although rare, will often be diagnosed after admission to a critical care unit for management of troublesome hypertension, hypokalemia, congestive heart failure, and various dysrhythmias. Suspicion of the diagnosis should always arise when these manifestations occur, particularly when hypokalemia is refractory to potassium supplementation. Without timely diagnosis and treatment, these patients will succumb to lethal dysrhythmias.

Absorption of micronized progesterone from a nonliquefying vaginal cream.

An improved delivery method to achieve sustained physiological P levels would be useful. Based on this single-dose pharmacokinetic study, micronized P prepared in a nonliquefying vaginal cream holds promise as a convenient method to achieve this goal with a single daily application.