AccessMyLibrary provides FREE access to millions of articles from top publications available through your library.
Under usual conditions, fluid balance is controlled primarily by release of arginine vasopressin, antidiuretic hormone (ADH), from the posterior pituitary gland. ADH acts on the kidney to increase reabsorption of water into the systemic circulation to maintain serum osmolality within relatively narrow limits; urine becomes more concentrated as water is conserved. Diabetes insipidus (DI) is a disorder associated with the kidneys' inability to concentrate urine, resulting in massive fluid loss and serum hyperosmolality.
The syndrome of DI results from either of two primary pathophysiologic conditions: (a) insufficient synthesis or release of an antidiuretic hormone (ADH) or (b) an abnormal renal response to ADH (Besunder, 1990). Infants and children, given limited fluid reserves, are especially sensitive to fluid and electrolyte imbalances. Individuals with DI who have limited access to water are often susceptible to severe dehydration resulting in serum hyperosmolality, seizures, and death. Therefore, DI in these populations may be life-threatening unless promptly diagnosed and treated. It is important that nurses be cognizant of contributing factors, signs and symptoms, and appropriate nursing management to intervene in a timely manner to prevent sequelae.
A variety of regulatory mechanisms control fluid balance to maintain plasma osmolality within a relatively narrow range. Stability of plasma concentration is controlled, in part, by hypothalamic centers that regulate thirst. The thirst mechanism stimulates intake of free water and stimulates ADH release. ADH is synthesized by the hypothalamus and stored in the posterior pituitary gland (Sklar, 1985). ADH stimulates the distal and collecting tubules of the kidneys to increase reabsorption of free water into the cardiovascular system, thus maintaining physiologic osmolality. Diminished levels of ADH result in increased urine output and excessive free water loss (Yucha & Suddaby, 1991) (see Figure 1).
Plasma osmolality appears to be the primary regulator of ADH secretion (Sklar, 1985). Synthesis and release of ADH is regulated by osmoreceptors within the brain that detect changes in extra-cellular osmolality (Shiminski-Maher, 1991). These osmoreceptors are sufficiently sensitive to changes in osmolality so that elevations as little as 2% of the serum osmolality value cause increased secretion of ADH to inhibit water losses and reduce osmolality.
Renal actions of ADH maintain serum osmolality within the range of 285-295 mOsm/L. A decline in osmolality rapidly reduces ADH release. When plasma osmolality is at or below 285 mOsm/L, ADH is suppressed, permitting the excretion of free water to increase serum osmolality. The effect is evident in the diuresis that results. Above the threshold of 295 mOsm/L, ADH is released in response to osmotic stimuli to produce water retention. ADH increases water reabsorption by increasing the permeability of the distal renal tubules and collecting ducts, thus producing water conservation. As levels of ADH increase, the urine volume declines, urine osmolality and specific gravity increase (Shiminski-Mayer, 1991). Retention of free water results in hemodilution and lowers the serum osmolality (Sklar, 1985).
Additional factors that affect ADH secretion are serum sodium levels and hemodynamic status. Reduced extracellular volume (ECV) with a concomitant elevation of serum sodium stimulates ADH secretion, whereas increased ECV reduces it. A reduction in blood volume by 10%, as with hemorrhage or dehydration, elicits secretion of ADH Sklar, 1985). As fluid imbalances are corrected, production and release of ADH are inhibited by a negative feedback mechanism from osmoreceptors to the posterior pituitary gland (Cagno, 1989).
DI is characterized by the inability to produce concentrated urine despite progressive serum hyperosmolality. DI can be categorized as either: (a) vasopressin sensitive, described as a neurogenic disorder (central DI) or (b) vasopressin resistant, or …