Diabetes Insipidus [Bell]

Title: Diabetes Insipidus [Bell]
Author: Bell, T. N.
Publisher: Critical Care Nursing Clinics of North America
Date Published: December 01, 1994
Reference Number: 85
When the critically ill patient's clinical course is complicated by diabetes insipidus, a significant threat to the equilibrium of the body's delicate water and electrolyte balance ensues. Patients with diabetes insipidus are at significant risk of dehydration, hypernatremia, alterations in level of consciousness, and hemodynamic instability from hypovolemia. This article presents the causes of, and pathophysiologic alterations in, central and nephrogenic diabetes insipidus. Clinical manifestations and therapeutic management of both conditions in the critical care population are described.

This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)

Diabetes insipidus (DI) is a condition characterized by the kidneys' inability to reabsorb body water as it flows through the kidney collecting ducts. Thus, the kidneys are unable to conserve body water and their ability to help maintain the body's delicate water and electrolyte balance is impaired. This is critical as body fluid volume, concentrations, and composition must be maintained within a narrow, precise range for basic bodily health.

The antidiuretic hormone (ADH) plays an important role in regulating body water balance. It is the body's failure to either produce, release, or respond to ADH that results in DI.

Osmolality is the concentration of osmotically active particles (e.g. salts, sugars, ions) in a solution. The solution can be a body fluid such as plasma or urine. When osmolality is high it means there is a greater ratio of particles to solvent than when osmolality is low. (Solvent is the liquid aspect of the solution, e.g. the water of body water minus the particles it carries.) The relation between plasma osmolality and urine osmolality helps determine the release of ADH.

When plasma osmolality reaches a certain level, it is detected by sensors in the hypothalamus. These sensors, called osmoreceptors, then signal the release of ADH. The ADH signals the kidneys to reabsorb water flowing through the kidney collecting ducts. This brings more water into the plasma, so plasma osmolality decreases, and it takes more water out of the urine, so the urine osmolality increases. Conversely, when plasma osmolality is low, ADH release is inhibited. Then, the kidneys do not reabsorb the water flowing through its collecting ducts, and more water is left in the urine, lowering its osmolality. In this way, excess body water is voided via dilute urine. It is the communication among osmoreceptors, sensing plasma concentrations of osmotically active particles (chiefly sodium), ADH and the kidneys that help regulate body water balance.

Bell discusses two forms of DI: pituitary DI (PDI) (also known as central DI or neurogenic DI) and nephrogenic DI (NDI). PDI results when the hypothalamus fails to produce and/or release ADH. In NDI, the hypothalamus produces and releases ADH in sufficient quantities, and sufficient quantities circulate in the plasma, but the kidneys cannot respond to the ADH. The person with either form of DI faces the same challenge to his body water balance. The kidneys' inability to reabsorb body water means an excess of water is lost via urination, which for DI patients is chronically excessive.

This results in plasma hyperosmolality: abnormally high concentrations of osmotically active particles, such as sodium, in the plasma, and abnormally low concentrations of osmotically active particles in the urine. Without adequate fluid to replace that lost through excessive urination, DI patients are at risk of fluid and electrolyte imbalance, dehydration and shock resulting from abnormally decreased plasma volume. The body's thirst center responds to this situation and the patient is chronically thirsty and must consume large volumes of water to compensate for the water lost through excessive urination. Infants and the elderly must be carefully monitored for they are often incapable of expressing their need for water.

Both forms of DI may either be acquired or inherited, temporary or permanent, partial (i.e. less severe symptoms) or complete (full symptoms). PDI is seen more frequently in critically ill people than NDI is seen. The primary causes of PDI are injuries in the hypothalamic region of the brain. The extent of the injury can often determine whether the PDI is temporary or permanent. Other causes of PDI include central nervous system infections, disease of the blood vessels of the brain, cerebral edema, faulty osmoreceptors, autoimmune diseases, intracranial hemorrhage and abnormal cellular growth in the brain. As mentioned, PDI may also be inherited.

NDI can be inherited, but is more commonly acquired, often as a consequence of some other disease or disorder such as kidney disease. Acquired NDI can be caused by electrolyte imbalance, protein starvation, long-term use of such prescription drugs such as lithium, demeclocycline, Amphotericin B, methoxyflurane, Getamicin, colchicine and loop diuretics. Sometimes even pregnancy can cause temporary NDI.

Since the symptoms are similar in both cases, diagnosticians must look to plasma levels of ADH to help distinguish between NDI and PDI. If there are low circulating levels of plasma ADH, it is indicative of PDI. Another way to distinguish between these two forms of DI is to monitor patient response to administration of a synthetically modified form of AVP called DDAVP after a carefully controlled period of water deprivation. Patients with PDI will respond by showing an increase in urine concentration; patients with NDI will not. Note, however, that this test only distinguishes between the complete forms of PDI and NDI.

PDI is managed by ensuring adequate water intake and administrating prepared ADH to compensate for the lack of naturally occurring ADH. The ADH substitute of choice is generally DDAVP. It goes into action within 1 hour after administration, and its effects last from 8 to 24 hours. In the case of NDI there is an adequate level of ADH, but it cannot be utilized. Therefore, NDI is managed by ensuring adequate water intake, maintaining a low sodium (and sometimes a low protein) diet, and treatment with thiazide diuretics. Thiazide diuretics help reduce urine volume, but they do have side-effects (such as robbing the body of potassium) and their use must be carefully monitored.