Sodium Disorders

Chapter 54 Sodium Disorders



Jamie M. Burkitt, DVM, DACVECC



KEY POINTS



• Most disorders of plasma sodium concentration result from abnormalities in the handling of water rather than sodium.

• Plasma sodium concentration is the major determinant of plasma osmolality.

• Hypernatremia or hyponatremia can cause central nervous system (CNS) disturbance resulting from changes in neuronal cell volume and function.

• Overly rapid correction of hypernatremia or hyponatremia can cause severe CNS dysfunction.

• Patients with hypernatremia or hyponatremia that require intravascular volume expansion should be treated with intravenous fluids that match their plasma sodium concentration.


INTRODUCTION


Sodium concentration is expressed as milliequivalents (mEq) of sodium per liter of serum or plasma. In the vast majority of cases, disorders of sodium concentration in dogs and cats result from abnormalities in water handling rather than an increased or decreased number of sodium molecules. To understand what determines plasma sodium concentration and how changes in plasma sodium concentration alter cellular function, one must understand the distribution of body water and the concept and determinants of osmolality.



Distribution of Total Body Water


Water makes up approximately 60% of an adult animal’s body weight; two thirds is intracellular and one third is extracellular. Extracellular water is distributed between the interstitial and intravascular compartments, which contain approximately 75% and 25% of the extracellular water, respectively (see Figure 64-1). The endothelium, which separates the intravascular fluid compartment from the interstitial space, and the cell membrane, which separates the interstitial and intracellular compartments, are freely permeable to water molecules. Therefore, in a closed system (no urinary or gastrointestinal (GI) output), when 1 L of free water (water containing no other molecules) is added to the animal, 666 ml will be distributed to the intracellular space and 333 ml to the extracellular space. Of the 333 ml added to the extracellular space, 250 ml will remain in the interstitial fluid space and 83 ml will be distributed to the intravascular compartment.



Osmolality and Osmotic Pressure


An osmole is one mole of any fully dissociated substance dissolved in water. Osmolality is the concentration of osmoles in a mass of solvent. In biologic systems, osmolality is expressed as mOsm/kg of water. Osmolarity is the concentration of osmoles in a volume of solvent, and in biologic systems is expressed as mOsm/L of water. Every molecule dissolved in the total body water contributes to osmolality, regardless of size, weight, charge, or composition. The most abundant osmoles in the extracellular fluid are sodium and potassium (and their accompanying anions chloride and bicarbonate), glucose, and urea. Hence, these molecules are the main determinants of plasma osmolality in healthy dogs and cats.


Plasma osmolality in healthy animals is approximated by the equation:



image



where Na+ = sodium, K+ = potassium, and BUN = blood urea nitrogen.


The blood urea nitrogen (BUN) and glucose concentrations are divided by 2.8 and 18, respectively, to convert them to mOsm/kg. As this equation shows, plasma sodium concentration is the major determinant of plasma osmolality.


Osmoles that do not cross the cell membrane freely are considered effective osmoles, whereas those that do cross freely are termed ineffective osmoles. The water-permeable cell membrane is functionally impermeable to sodium and potassium. As a result, sodium and potassium molecules are effective osmoles and they exert osmotic pressure across the cell membrane. The net movement of water into or out of cells is dictated by the osmotic pressure gradient. Osmotic pressure causes water molecules from an area of lower osmolality to move to an area of higher osmolality until the osmolalities of the compartments are equal.


When sodium is added to the extracellular space at a concentration greater than that in the extracellular fluid, intracellular volume decreases (the cell shrinks) as water leaves the cell along its osmotic pressure gradient. Conversely, cells swell when free water is added to the interstitial space and water moves intracellularly along its osmotic pressure gradient.



Regulation of Plasma Osmolality


Hypothalamic osmoreceptors sense changes in plasma osmolality, and changes of only 2 to 3 mOsm/kg induce compensatory mechanisms to return the plasma osmolality to its hypothalamic setpoint.1 The two major physiologic mechanisms for controlling plasma osmolality are the antidiuretic hormone (ADH) system and thirst.



Antidiuretic Hormone


ADH is a small peptide secreted by the posterior pituitary gland. There are two major stimuli for ADH release: elevated plasma osmolality and decreased effective circulating volume. Increased plasma osmolality causes shrinkage of a specialized group of cells in the hypothalamus called osmoreceptors. When their cell volume decreases, these hypothalamic osmoreceptors send impulses via neural afferents to the posterior pituitary, leading to ADH release.2 When effective circulating volume is low, baroreceptor cells in the aortic arch and carotid bodies send neural impulses to the pituitary gland that stimulate ADH release.


In the absence of ADH, renal tubular collecting cells are relatively impermeable to water. When ADH activates the V2 receptor on the renal collecting tubular cell, aquaporin-2 molecules are inserted into the cell’s luminal membrane. Aquaporins are channels that allow the movement of water into the renal tubular cell. Water molecules cross through these aquaporins into the hyperosmolar renal medulla down their osmotic gradient. If the kidney is unable to generate a hyperosmolar renal medulla because of disease or diuretic administration, water will not be reabsorbed, even with high concentrations of ADH. Thus, circulating ADH concentration and ADH’s effect on the normal kidney are the primary physiologic determinants of free water retention and excretion.



Thirst


Hyperosmolality and decreased effective circulating volume also stimulate thirst. The mechanisms by which hyperosmolality and hypovolemia stimulate thirst are similar to those that stimulate ADH release. Thirst and the resultant water consumption are the main physiologic determinants of free water intake.



Prioritization of Osmolality and Effective Circulating Volume


Under normal physiologic conditions, the renin-angiotensin-aldosterone system monitors and fine tunes effective circulating volume, and the ADH system maintains normal plasma osmolality. However, maintenance of effective circulating volume is always prioritized over maintenance of normal plasma osmolality. Therefore patients with poor effective circulating volume will have increased thirst and ADH release regardless of their osmolality. The resultant increased free water intake (from drinking) and water retention (from ADH action at the level of the kidney) can lead to hypoosmolality in patients with poor effective circulating volume. An example of the defense of effective circulating volume at the expense of normal plasma osmolality is seen in patients with chronic congestive heart failure that present with hyponatremia.3



Total Body Sodium Content Versus Plasma Sodium Concentration


Plasma sodium concentration is different than, and independent of, total body sodium content. Total body sodium content refers to the total number of sodium molecules in the body, regardless of the ratio of sodium to water. Sodium content determines the hydration status of the animal. As it is used clinically, hydration is a misnomer, because findings such as skin tenting and moistness of the mucous membranes and conjunctival sac are determined by the sodium content and the water that those sodium molecules hold in an animal’s interstitial space.


When patients have increased total body sodium, an increased quantity of fluid is held within the interstitial space and the animal appears overhydrated, regardless of the plasma sodium concentration. Overhydrated patients may manifest a gelatinous subcutis, peripheral, or ventral pitting edema, chemosis, or excessive serous nasal discharge.


When patients have decreased total body sodium, a decreased quantity of fluid is held within the interstitial space and the animal appears dehydrated, regardless of the plasma sodium concentration. Once a patient has lost 5% or more of its body weight in isotonic fluid (≥5% dehydrated), it may manifest decreased skin turgor, tacky or dry mucous membranes, decreased fluid in the conjunctival sac, or sunken eye position. Patients that are less than 5% dehydrated appear clinically normal. Patients with dehydration can become hypovolemic as fluid shifts from the intravascular space into the interstitial space as a result of decreased interstitial hydrostatic pressure.


The sodium-to-water ratio is independent of the total body sodium content: patients may be normally hydrated, dehydrated, or overhydrated (normal, decreased, or increased total body sodium content) and have a normal plasma sodium concentration, hypernatremia, or hyponatremia.



HYPERNATREMIA


Hypernatremia is defined as plasma or serum sodium concentration above the reference interval. Hypernatremia is common in critically ill dogs and cats.



Etiology


Most dogs and cats with hypernatremia have increased free water loss rather than increased sodium intake or retention.



Free Water Deficit


Normal animals can become severely hypernatremic if denied access to water for extended periods. Animals with vomiting, diarrhea, or polyuria of low-sodium fluid may also develop hypernatremia. Diabetes insipidus (DI), a syndrome of inadequate release of or response to ADH, can cause hypernatremia (see Chapter 70, Diabetes Insipidus). Animals with DI become severely hypernatremic when they do not drink water, because they cannot reabsorb free water in the renal collecting duct. Acute or critical illness can unmask previously undiagnosed DI.4 A syndrome of hypodipsic hypernatremia has been reported in Miniature Schnauzers,5-7 one of which was diagnosed with congenital holoprosencephaly.5 This syndrome is most likely due to impaired osmoreceptor or thirst center function. In other dog breeds and cats, hypodipsic hypernatremia has been associated with hypothalamic granulomatous meningoencephalitis, hydrocephalus, and other central nervous system (CNS) deformities and CNS lymphoma.8-12


Diagnostic differentiation between central DI, nephrogenic DI, and hypodipsic hypernatremia can be complex and is outside the scope of this chapter. The reader is referred to more detailed texts for further information.13-15

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Sodium Disorders

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