Pathophysiology
Summary
In the human body, water and solutes are broadly compartmentalized into the intracellular and extracellular compartments. Approximately ⅔ of the total body water and solutes are located intracellularly, with the remaining ⅓ located extracellularly. Osmolality, primarily determined by sodium levels, is the driving force for fluid movement between these compartments, and is normally 285-295 mOsm.
Various conditions can disrupt this balance, each leading to specific physiological consequences. For example, secretory diarrhea causes hypovolemic normonatremia by reducing blood volume while maintaining sodium levels. In contrast, SIADH induces euvolemic hyponatremia, retaining free water and thereby diluting sodium without altering blood volume. Medications like diuretics or adrenal insufficiency can lead to hypovolemic hyponatremia, where sodium loss exceeds water loss.
Conditions that result in a loss of water greater than sodium, such as in vomiting or osmotic diuresis, serum sodium and osmolality are both increased. This results in contraction of both intracellular and extracellular spaces, manifesting as hypovolemic hypernatremia. Conversely, diseases such as CHF and nephrotic syndrome can cause relative hypovolemia, where total body volume is increased but intravascular volume is decreased, leading to secondary aldosteronism and activation of the RAAS and ADH systems. This leads to hypervolemic hyponatremia, where both the intracellular and extracellular compartments are expanded, but serum osmolality is decreased.
Administering hypertonic saline or sodium bicarbonate can overload sodium, resulting in contraction of the intracellular space and expansion of the extracellular space, culminating in hypervolemic hypernatremia. In states of significant hyperglycemia, like diabetic ketoacidosis (DKA), increased serum osmolality contracts both cellular compartments, leading to hypovolemic hyperosmolality.
Symptoms of hyponatremia range from confusion & nausea to severe complications like cerebral edema, seizures, & coma. Rapid correction of hyponatremia can result in osmotic demyelination syndrome, which can cause significant neurological impairment and potentially lead to locked-in syndrome in extreme cases.
Lesson Outline
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FAQs
Sodium is the primary determinant of serum osmolality, which is the concentration of dissolved solutes in the blood. As the major extracellular cation, sodium, along with its conjugate anions chloride and bicarbonate, significantly influences osmolality. Under normal conditions, serum osmolality ranges from 285-295 mOsm. Serum osmolality can be roughly estimated by doubling the serum sodium concentration.
Osmolality serves as the driving force for the movement of water between the body's fluid compartments, including the intracellular and extracellular spaces. Water moves freely until an osmotic equilibrium is established. Changes in osmolality cause shifts in fluid distribution; an increase in osmolality will draw water into the compartment, while a decrease will lead to fluid exiting the compartment.
Loss of isotonic fluid, such as in secretory diarrhea, leads to a contraction of the extracellular fluid volume. Because serum sodium and osmolality remain stable in this situation, the intracellular volume is unaffected. The end result is a state known as hypovolemic normonatremia, where the extracellular volume is reduced but sodium levels are normal.
Cirrhosis and nephrotic syndrome both impair albumin production, leading to low serum oncotic pressure. This causes intravascular volume depletion as fluid moves into the interstitial space, resulting in conditions like ascites and edema. Despite the increased total body volume, the intravascular compartment is depleted, which can activate the renin-angiotensin and ADH systems, leading to further fluid retention.
Hyponatremia manifests with symptoms like confusion, altered mental status, lethargy, and in some cases, nausea and vomiting. Severe instances can cause cerebral edema due to water shifting into neurons, leading to seizures and coma. Rapid correction of hyponatremia is risky; it can cause water to move quickly out of cells, leading to osmotic demyelination syndrome. This severe neurological dysfunction can result in paralysis or a 'locked-in syndrome' where voluntary movement is severely restricted.
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