Correction of Water, Electrolyte, and Acid-Base Derangements by Hemodialysis and Derived Techniques

Sodium Abnormalities

Dysnatremias (hypo- and hypernatremia) are common in patients admitted to the ICU with prevalence approaching 20% to 30%. Even mild degrees of hyponatremia and hypernatremia confer markedly increased risk for mortality and increased length of stay. Sodium is the principal determinant of plasma and dialysate osmolality, and the use of IHD can affect dramatically a patient's osmotic homeostasis. As water flows from an area of lower osmolality to one of higher osmolality, the associated fluid shifts can affect hemodynamic stability adversely (when water moves from intravascular to tissue compartments), cerebral fluid and osmolyte homeostasis (when fluid shifts in either direction), or both. Sodium crosses hemodialysis membranes by means of diffusion or convection. Diffusion depends on the concentration gradient and the molecular weight of the solute, but not all ionized sodium is diffusible. The presence of negatively charged plasma proteins results in some cation retention to maintain electrical neutrality (the Donnan effect). However, the ionized sodium in the dialysate is completely available for diffusion, because there are no anionic proteins there. Because of this discrepancy, a diffusive gradient of zero can be achieved only by choosing an ionized sodium concentration in the dialysate of about 5 to 10 mEq/L less than the ionized sodium concentration in plasma water. Other factors that may change the amount of sodium available for diffusion are dialysate temperature and pH, and the addition of other ions, such as carbonate, bicarbonate, and phosphate. In contrast, convective transport (ultrafiltration) of sodium occurs when plasma water is driven across the membrane by either a hydrostatic or an osmotic force.

The choice of dialysate sodium concentration depends on the goals to be achieved and has changed over the years. In the past, a lower dialysate sodium concentration, typically less than 135 mEq/L, was used to limit interdialytic hypertension and thirst. This approach, however, can be complicated by headaches, muscle cramps, nausea, and vomiting and may play a role in the dialysis dysequilibrium syndrome. The use of a dialysate sodium concentration below the serum sodium concentration results in fluid shifts from the extracellular compartment to the intracellular compartment, because diffusion lowers serum sodium and plasma osmolality. Ultimately, the total water loss from the extracellular space exceeds the total water loss from the body. In contrast, the use of a dialysate with a higher sodium concentration than the serum sodium concentration causes water removal from intracellular and extracellular compartments and minimizes the effect of plasma volume loss.

The mechanism by which higher dialysate sodium concentration maintains a greater proportion of plasma volume while accomplishing ultrafiltration is especially important in the context of AKI. Many patients with AKI are hypervolemic but are also hypotensive from cardiogenic or septic shock, and the ability to produce significant ultrafiltration while minimizing hemodynamic impact is an important tool in such cases. The improvement in hypertension control and reduced thirst associated with lower dialysate sodium are optimal in the outpatient setting. However, in the critically ill patient, thirst is less relevant, and hypotension may be detrimental. For this reason, the use of a dialysate sodium concentration of 140 to 145 mEq/L often is advised for acute dialysis, and the same principle underlies the use of sodium modeling to prevent or manage intradialytic hypotension.

Hemodialysis of a patient with an abnormally low or elevated serum sodium concentration deserves special consideration. Dialysis is not used typically to treat these conditions but is often necessary in patients with AKI in whom dysnatremias have developed, or in critically ill patients with ESRD. The correct approach to acute dialysis of a patient with significant hyponatremia or hypernatremia depends on the severity and chronicity of the dysnatremia, and dialysis should never be initiated in such a patient without careful consideration of both factors. Hyponatremia, a common complication in the critically ill patient, is usually asymptomatic but can cause central nervous system manifestations, generally at serum sodium concentrations below 125 mEq/L. The correction of hyponatremia can be complicated by osmotic demyelination if the serum sodium concentration is raised rapidly in the setting of chronic hyponatremia (with associated cerebral accommodation to hypotonicity). Even in the symptomatically hyponatremic patient, it generally is believed that a targeted extent of correction should not exceed 8 to 10 mmol/L in the first 24 hours but may have a lower rate of correction (4-6 mmol/L in 24 hours) in select clinical situations, such as malnutrition, alcohol liver disease, and hypokalemia. Similarly, patients with severe, symptomatic hyponatremia should be treated with 3% saline given as 100-mL bolus(es) to raise the plasma sodium concentration rapidly by 4 to 6 mmol/L, to achieve clinical improvement, followed by slower correction. In the setting of asymptomatic hyponatremia, there is no indication for acute correction, and the targeted rate of correction should not exceed 8 to 10 mmol/L/day. During a typical average-efficiency, 4-hour hemodialysis session, the expected postdialysis serum sodium concentration is typically at the midpoint between the predialysis serum sodium concentration and the dialysate sodium concentration. Because the change in serum sodium generated with this IHD may be too rapid, it may become necessary to use a lower dialysate sodium concentration, shorter dialysis time, or a slower blood flow rate to dialyze the patient safely. Accordingly, more frequent dialysis may be necessary to achieve adequate clearance for azotemia control or hyperkalemia while safely correcting hyponatremia. If overcorrection occurs with hemodialysis, intravenous dextrose or free water administration may be required to restore the serum sodium to the desired target level.

A similar approach is necessary in the hypernatremic patient undergoing dialysis. In patients with elevated serum sodium levels that have developed suddenly (over the course of hours), rapid correction (1 mmol/L/hr) is recommended and is associated with minimal side effects. However, in the patient with hypernatremia of prolonged or unknown duration, an accumulation of organic solutes in the brain cells requires several days to dissipate. The maximal rate of correction in chronic hypernatremia should not exceed 0.5 mmol/L/hr, with a targeted drop in serum sodium concentration of up to 10 mmol/L/day. As described previously, the use of a dialysate sodium concentration below the serum sodium concentration can be complicated by hemodynamic instability, as fluid shifts from the extracellular to the intracellular compartment and the plasma volume contracts. Therefore the use of a dialysate sodium concentration similar to that found in the serum, and slow correction of the hypernatremia with hypotonic intravenous fluids generally is recommended.

However, there are several published case reports describing the rapid correction of hypernatremia with hemodialysis. In one report, three patients with severe hypernatremia and volume overload were treated with low dialysate sodium concentrations (110 mEq/L), causing reductions in serum sodium of 19 to 34 mEq/L over the course of 3.5 to 4 hours. Other reports have described the use of IHD, one with a dialysate sodium of 138 mEq/L in a hypovolemic hypernatremic patient who required daily 2-hour treatments, and the other in burn patients with hypernatremic AKI. Despite the lack of neurologic complications seen in these selected patients, large changes in serum sodium concentrations are best avoided over the time span of IHD. Correction of severe hypernatremia with renal replacement therapy (RRT) is probably more safely achieved with less efficient, more titratable techniques, such as sustained low-efficiency daily dialysis (SLEDD) or continuous RRT.