Diabetes Insipidus and Syndrome of Inappropriate Antidiuretic Hormone in Critically Ill Patients

Depending upon the age and sex of a human, water constitutes 55% to 80% of the body’s weight and provides a milieu vital for survival. Water imbalance is common among the critically ill. Excessive increases or decreases in body water can be lethal. There are numerous pathologic and iatrogenic causes for water imbalance, the most troublesome being disorders of antidiuretic hormone (ADH) secretion. Antidiuretic hormone plays a pivotal role in conserving water by increasing reabsorption of water by the kidney. Without the influence of ADH (as is seen in diabetes insipidus), a person would be required to ingest between 5 and 15 L of water daily to match urinary losses. Conversely, excessive ADH secretion would reduce urine output in adults to as little as 500 mL per day, dangerously diluting blood volume and expanding intracellular volume. This is what causes the symptoms of the syndrome of inappropriate ADH (SIADH). The care of patients who are critically ill and have disorders of ADH secretion can be challenging. The challenge lies in the recognition and treatment of the disorder. A collaborative team approach helps patients achieve and maintain the delicate balance of body fluids

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Syndrome of Inappropriate Antidiuretic Hormone and Cerebral Salt Wasting in Critically Ill Patients

AACN Advanced Critical Care ◽

10.1097/nci.0b013e318267f0c8 ◽

2012 ◽

Vol 23 (3) ◽

pp. 240-241

Author(s):

&NA;

Keyword(s):

Antidiuretic Hormone ◽

Critically Ill ◽

Critically Ill Patients ◽

Cerebral Salt Wasting ◽

Salt Wasting

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Syndrome of Inappropriate Antidiuretic Hormone and Cerebral Salt Wasting in Critically Ill Patients

AACN Advanced Critical Care ◽

10.4037/nci.0b013e31824ebd1b ◽

2012 ◽

Vol 23 (3) ◽

pp. 233-239

Author(s):

Amanda Zomp ◽

Earnest Alexander

Keyword(s):

Antidiuretic Hormone ◽

Critically Ill ◽

Critically Ill Patients ◽

Cerebral Salt Wasting ◽

Salt Wasting

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Thirst in Critically Ill Patients: From Physiology to Sensation

American Journal of Critical Care ◽

10.4037/ajcc2013533 ◽

2013 ◽

Vol 22 (4) ◽

pp. 328-335 ◽

Cited By ~ 35

Author(s):

Shoshana Arai ◽

Nancy Stotts ◽

Kathleen Puntillo

Keyword(s):

Antidiuretic Hormone ◽

Critically Ill ◽

Critically Ill Patients ◽

Essential Role ◽

Plasma Osmolality ◽

Compensatory Mechanism ◽

Volume Loss ◽

Water Regulation ◽

Adrenergic Agonists ◽

Renin Angiotensin Aldosterone System

Critically ill patients often report distressful episodes of severe thirst, but the complex biochemical, neurohormonal mechanisms that regulate this primal sensation still elude clinicians. The most potent stimuli for thirst are subtle increases in plasma osmolality. These minute changes in osmolality stimulate central osmoreceptors to release vasopressin (also known as antidiuretic hormone). Vasopressin in turn acts on the kidneys to promote the reabsorption of water to correct the increased osmolality. If this compensatory mechanism fails to decrease osmolality, then thirst is triggered to motivate drinking. In contrast, thirst induced by marked volume loss, or hypovolemic thirst, is subject to the tight osmoregulation of the renin-angiotensin aldosterone system and accompanying adrenergic agonists. Understanding the essential role that thirst plays in salt and water regulation can provide clinicians with a better appreciation for the complex physiology that underlies this intense sensation.

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