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Introduction

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Critically ill patients are prone to a wide variety of fluid, electrolyte, and acid-base disorders. Two of those disorders are of particular relevance to patients with critical neurologic illness: hyponatremia and hypernatremia. These are by far the most common electrolyte abnormalities in patients with central nervous system disease and have the most pressing diagnostic and therapeutic implications. This chapter therefore will focus exclusively on these disorders. Interested readers will find a recent, more comprehensive discussion of fluid, electrolyte, and acid-base abnormalities in critically ill patients elsewhere.1

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Hypo- and hypernatremia are manifestations of impaired water homeostasis. They occur frequently in patients with central nervous system disease2 and are associated with increased morbidity and mortality rates.3, 4

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Plasma sodium concentration (PNa) normally varies very little. This tight regulation of the PNa depends on the following elements: (1) modulation of pituitary secretion of arginine vasopressin (AVP; also known as antidiuretic hormone, or ADH) over a wide range in response to physiologic stimuli, (2) kidneys that are capable of responding to circulating AVP by varying the urine concentration, (3) intact thirst, and (4) access to water.

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The normal response to water ingestion (of sufficient magnitude to lower the plasma osmolality even slightly) is the excretion of maximally dilute urine (urine osmolality < 100 mOsm/kg). The underlying physiologic sequence is as follows: the plasma hypo-osmolality is sensed by the cells comprising the hypothalamic osmostat. These hypothalamic nuclei then proportionately reduce their synthesis of AVP, leading to diminished AVP release into the circulation by the posterior pituitary. The lower circulating AVP concentration causes less vasopressin receptor type 2 (V2 receptor) stimulation of the epithelial cells lining the renal collecting duct. This, in turn, results in the insertion of proportionately fewer water channels into the collecting duct, creating a more water-impermeable conduit, which allows excretion of the dilute urine elaborated by the more proximal segments of the nephron.5

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Conversely, plasma hyperosmolality leads to higher circulating AVP concentration and proportionately higher water permeability of the collecting duct, and the excretion of a concentrated urine.5

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Figure 43-1 shows the relationship between plasma osmolality, plasma AVP concentration, and urine osmolality. The normal “set point” is a plasma osmolality of about 285 mOsm/kg. Notice that the minimum urine osmolality is about 50 mOsm/kg, and the maximum about 1200 mOsm/kg.6 When plasma osmolality rises beyond 290 to 295 mOsm/kg, the thirst center of the hypothalamus is stimulated. At that point, neurologically intact individuals with access to water will drink until the plasma osmolality returns to normal.6

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Figure 43-1.

Relationship between plasma osmolality, plasma adenosine vasopressin concentration, and urine osmolality. PAVP', plasma arginine vasopressin concentration; Posm, plasma osmolality; Uosm, urine osmolality.

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It is important to recognize that plasma osmolality is not the only determinant of AVP synthesis and release. Low arterial blood pressure and low effective arterial volume powerfully stimulate AVP release.6 This baroreceptor-mediated AVP release is teleologic, since water retention is an important component in the defense against hypovolemia. So primal is this circulatory defense that the baroreceptor ...

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