Fluid and Metabolic Derangements

Metabolic derangements are frequent in patients with severe central and peripheral neurological illnesses. These alterations may occur as part of the critical illness itself or as sequelae of a number of treatments for acute neurological problems. Many of these disorders are not clinically obvious until they become severe. For these reasons, monitoring of metabolic parameters and strategies to maintain fluid and electrolyte balance have become a routine parts of intensive care unit (ICU) protocols, and neurological illnesses are no exception.

PHYSIOLOGY OF SODIUM AND WATER BALANCE

Water comprises approximately 50% to 60% of the human body weight and is distributed in extracellular fluid (ECF) and intracellular fluid (ICF) compartments. About 55% to 75% of body water is intracellular, and the remaining 25% to 45% is extracellular, divided between the intravascular plasma fraction and interstitial spaces.

The particle, or solute, concentration in fluid is referred to as osmolality, and is expressed in milliosmoles per kilogram (mOsmol/kg) of fluid. Water tends to be freely permeable across cell membranes, resulting in an equilibration between the ICF and ECF osmolalities. However, the solutes in ECF and ICF are vastly different based on differential membrane permeabilities and active transport mechanisms. The major ECF particles are Na and the associated anions, Cl and HCO₃, whereas the ICF contains predominantly K and organic anions. Sodium is largely restricted to the ECF, therefore, it is the dominant contributor to tonicity. Its concentration also reflects ECF volume and can be used as a surrogate measure of that volume. The concentration of the intracellular particles (K and associated anions) are held fairly constant, for which reason changes in the osmolality of the ICF are most often a reflection of changes in ICF water, usually driven by an equilibration with ECF osmolality. Brain cells apparently lose or generate effective osmoles to defend against major fluid shifts in some situations. The added “idiogenic osmoles” alluded to in Chapter 3 in relation to brain swelling are most prone to arise in chronic circumstances of hyponatremia, hypernatremia, and hyperglycemia. This osmotic adaptation occurs slowly and requires the synthesis or transport of solutes.

Water Balance

Normal plasma osmolality is maintained between 275 and 290 mOsmol/kg. Homeostatic mechanisms sense a 1% to 2% change in tonicity and drive the maintenance of water balance as long as water intake exceeds the minimal physiological requirements. Water intake is normally stimulated by thirst, resulting from either hypertonicity or hypovolemia. Osmoreceptors in the anterolateral hypothalamus are sensitive to a rise in tonicity, the thirst threshold being approximately 295 mOsmol/kg. Freely permeable osmoles such as urea or glucose have little effect on the thirst threshold (1).

Water intake normally exceeds physiological needs and water balance; therefore, it is tightly maintained by renal water excretion and largely controlled by arginine vasopressin (AVP) and antidiuretic hormone (ADH). As is well known, AVP is synthesized in the hypothalamus and secreted by the posterior pituitary. Binding of AVP to receptors in the renal collecting tubules stimulates water reabsorption. Other factors facilitate AVP release, including hypovolemia, pain, nausea, stress, hypoglycemia, and various drugs.

Sodium Balance

Sodium (Na) intake is generally in excess of the physiological sodium requirements. Excessive dietary intake of Na increases ECF volume, leading to a renal response of enhanced sodium excretion.

The renin-angiotensin-aldosterone system and sympathetic activity promote Na retention, whereas a natriuretic system fosters Na excretion. Baroreceptors that sense decreased intravascular volume and reduced blood pressure are the main stimuli for the release of renin. Other receptors monitor Na concentration in the nephron and modulate renin release. Renin leads to production of angiotensin II, via angiotensinogen and angiotensin, resulting in aldosterone release from the adrenal medulla. Angiotensin II stimulates thirst, aldosterone leads to Na resorption, and renal sympathetic activity also promotes Na retention (2). The factors favoring Na retention are countered by a natriuretic system that is less well understood. Atrial natriuretic factor (ANF), released from the heart in response to increased cardiac filling pressures, inhibits Na resorption (3,4). Atrial natriuretic factor is found in brain also, mainly in perihypothalamic regions, and it (as well as other central factors) appears to be involved in Na homeostasis (5).

TABLE 6.1. Characteristics of commonly seen fluid and electrolyte disturbances in neurocritical patients

	Vascular volume	Serum sodium	Urine sodium	Urine osmolality
Diabetes insipidus	↓	↑	↔	↓
SIADH	↔↑	↓	↔↑	↑
Cerebral salt wasting	↓	↓	↑	↔↑
SIADH, syndrome of inappropriate antidiuretic hormone.

CLINICAL DERANGEMENTS OF WATER AND SODIUM BALANCE IN THE NEUROLOGICAL INTENSIVE CARE UNIT

Disorders occur in various combinations of volume status and sodium concentration (Table 6.1) because water and sodium are independently regulated. This is the case as well when therapies such as hyperosmolar treatment create or exacerbate these disorders.

Hyponatremia

Hyponatremia is the result of excess ECF water in relation to Na. This circumstance occurs in relation to excess total body sodium in congestive heart failure. In contrast, normal Na with excess free water result from inappropriate ADH, and with decreased Na, in salt-wasting syndromes (natriuresis). The clinical distinction among these three states depends on an understanding of the time course, volume status, and associated medical conditions (Fig. 6.1). In the neurocritical care setting, a steady-state of water balance is rarely allowed since intravenous fluids and interventions are common. It may be difficult to determine if the disorder would lead to decreased volume without intervention. Slowly evolving perturbations can be significant yet clinically silent; for example, chronic hyponatremia often reaches levels of 110 to 115
mEq/L without symptoms. Lower levels, or acute reductions of Na below 125 mEq/L, generally are associated with somnolence, confusion, or seizures. Moreover, seizures resulting from this degree of hyponatremia are refractory to anticonvulsants.

FIG. 6.1. Clinical algorithm for evaluation of hyponatremia.

Hypernatremia

Hypernatremia usually results from water loss, or occasionally from sodium excess (Fig. 6.2). Mild hypernatremia (serum Na less than 160 mEq/L) is frequent and usually well tolerated in the neurocritical care setting. Profound hypertonic states with Na greater than 160 can be associated with confusion, lethargy, and seizure, and excessive mortality is associated with serum Na greater than 180 mEq/L.

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