Disorders Of Water Imbalance

Emerg Med Clin N Am 23 (2005) 749–770

Disorders of Water Imbalance
Michelle Lin, MDa,*, Stephen J. Liu, MDb, Ingrid T. Lim, MDb
San Francisco General Hospital Emergency Services, University of California San Francisco, 1001 Potrero Avenue, Suite 1E21, San Francisco, CA 94110, USA b Stanford-Kaiser Emergency Medicine Residency Program, 701 Welch Road, Building C, Palo Alto, CA 94304-5777, USAa

Lightheadedness, nausea, headache, fatigue, and confusion are nonspecific symptoms that may be consistent with either hyponatremia or hypernatremia. Such subtle presentations of water imbalance contrast their potentially devastating neurologic sequelae, which may be caused by the disorders themselves or iatrogenically by overly aggressive fluid resuscitation. In the emergency department (ED),two questions frequently arise regarding these conditions. First, when should such a disorder be suspected in a patient? Second, what type of intravenous fluids, if any, should be given and at what rate to correct the water imbalance? To address these issues, a basic understanding of water and sodium cellular physiology is crucial. There are three fundamental principles that will be highlighted.1. Water freely shifts between the intracellular and extracellular space to maintain osmotic equilibrium. Body fluid can be divided into intracellular and extracellular compartments, separated by a solute-impermeable, but water-permeable, membrane barrier. Water diffuses freely across this membrane barrier, allowing osmolality, defined as the ratio of solute to free water, to remain constant betweenthese two spaces. The predominant effective solute in the extracellular space is sodium, and its serum concentration closely reflects plasma osmolality. 2. A normal kidney will attempt to reabsorb or excrete solute-free water to preserve a normal plasma osmolality of 275 to 290 mOsm/kg. The primary hormone regulating plasma osmolality is arginine vasopressin,

* Corresponding author. E-mailaddress: milin@itsa.ucsf.edu (M. Lin). 0733-8627/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.emc.2005.03.001 emed.theclinics.com

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also known as antidiuretic hormone (ADH). It is synthesized in the hypothalamus and released into the systemic circulation by means of the posterior pituitary gland [1]. Despite wide fluctuations in water and sodiumintake, the body normally can maintain serum osmolality in a narrow range (275 to 290 mOsm/kg) [2]. Osmoreceptors near the hypothalamus sense plasma osmolality and modulate vasopressin release [3,4]. Vasopressin functions at the distal collecting duct of the kidney to increase water reabsorption in this otherwise relatively waterimpermeable section of the nephron [5]. In hypo-osmolar conditionsfor instance, vasopressin levels fall to a low basal rate to reabsorb less free water, resulting in more dilute urine. In addition to changes in plasma osmolality, hypotension and hypovolemia also may trigger vasopressin release, which potentially may worsen a hypo-osmolar state. Other nonosmotic triggers for vasopressin release include pain, nausea, and acidosis [6,7]. The thirst stimulus providesanother crucial, but less sensitive, means for the body to maintain water homeostasis by promoting oral intake of free water. Similar to vasopressin release, thirst also can be triggered by hypotension and hypovolemia [8]. 3. Rapid transcellular shift of water can lead to cellular damage, particularly in the central nervous system (CNS). In a normal steady-state environment, free water diffuses inand out of the intracellular space to maintain osmotic equilibrium. With the significant fluid shifts associated with hyponatremia and hypernatremia, however, major cellular volume changes can lead to cell damage and cell death, particularly in the CNS, resulting in irreversible neurologic injury. As an initial compensatory mechanism to preserve cellular volume, there is a rapid shift of sodium,...