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Description
Major advances in dialysis treatment for end stage renal disease have occurred in the last 30 years; and while there have been major improvements in both technology and technique, there remains considerable intra/interdialytic morbidity (Bonomini, Coli, & Scolari, 1997; Churchill, 1996; Oliver, Edwards, & Churchill, 2001; Palmer, 2001; Petitclerc & Jacobs, 1995; Sadowski, Allred, & Jabs, 1993; Sang, Kovithavongs, Ulan, & Kjellstrand, 1997; Sherman, 2001; Stiller, Bonnie-Scorn, Grassman, UhlenbuschKorwer, & Mann, 2001). This morbidity has been described since the early 1960s and includes a variety of symptoms that may be attributed to physiological changes induced by the process of hemodialysis (Arieff, 1994; Tang et al., 2006).
The symptoms are given different names throughout the literature, including dialysis intolerance, dialysis disequilibrium syndrome, vascular instability syndrome, and dialysis fatigue. For the purpose of this article, the term dialysis intolerance will be used.
Symptoms of dialysis intolerance may present as headache, light-headedness, nausea, vomiting, muscle cramps, and hypotension either during or after the hemodialysis session. The pathophysiological explanation for these symptoms, while multifactorial, remains somewhat unclear, but the following appears to be a generally accepted description of the process among leading researchers (Bonomini, 1995; Levin & Goldstein, 1996; Movilli et al., 1997; Petitclerc & Jacobs, 1995; Sang et al., 1997; Stiller et al., 2001). The total amount of water in the body is approximately 60% of the adult human body weight. Total body water is divided between the extra-cellular fluid (ECF) and the intracellular fluid (ICF) compartments. These two compartments differ in their electrolyte composition, with sodium being the main cation of the ECF. Equilibrium is maintained throughout the body compartments by way of osmotic equilibration and the permeability of the cell membranes (Stiller et al., 2001).
The two processes that play a major role in dialysis intolerance are solute disequilibrium and blood volume depletion (Bonomini et al., 1997). During a dialysis session, fluid is removed via ultrafiltration primarily from the extracellular compartment, thereby reducing the plasma volume and inducing ECF volume contraction (Levin & Goldstein, 1996; Petitclerc & Jacobs, 1995). The body attempts to compensate for this plasma volume depletion by refilling from the ICF but cannot always keep pace. This fluid shift depletes the available fluid and symptoms occur such as those described above.
Accompanying this process, there is also a rapid decline in solutes (primarily urea) during the initial stage of dialysis, inducing a fall in plasma osmolality (Levin & Goldstein, 1996). This rapid decline in urea causes disequilibrium between the ECF and the ICF, resulting in water moving from the extracellular compartment to the intracellular compartment, which may result in neuronal overhydration and the associated symptoms of dialysis intolerance (Stiller et al., 2001).
Some evidence suggests that autonomic dysfunction, decreased cardiac reserve, changes in serum potassium and calcium concentrations and more recently, accumulation of nitric oxide also play a part in the presence of adverse symptoms during and after dialysis therapy (Dheenan & Henrich, 2001).
History
Historically, patients were dialyzed against hyponatremic dialysate (a sodium level of 130-135 mEq/1) on the assumption that this would inhibit sodium accumulation interdialytically, thus preventing hypertension (Kelly, 1996; Palmer, 2001). While this strategy allowed patients to be dialyzed down to dry weight without any significant morbidity, session times were typically 8 to 10 hours long (Kelly, 1996).
Further technological advances and the advent of hollow fibre dialyzers in the late 1980s, allowed dialysis times to be reduced, but patients typically experienced signs and symptoms of dialysis intolerance (Kelly, 1996; Parker, 2000). This was and remains largely due to the rapid removal of plasma volume without adequate refilling with concomitant decreases in blood sodium and osmolality described above (Coli et al., 1998; Kelly, 1996; Sang et al., 1997).
Researchers at this time identified that the symptoms of dialysis intolerance were reduced and hemodynamic stability improved by increasing the dialysate sodium (Kelly, 1996; Palmer, 2001). This was offset against high post-dialysis serum sodium and increased thirst, potentially leading to the development of long term complications such as left ventricular hypertrophy and congestive cardiac failure (Palmer, 2001).
Ultrafiltration profiling was another method that, at this time, was considered to reduce the hypotension commonly seen towards the end of the dialysis session. It was deduced that if the majority of the fluid removal took place in the beginning of the dialysis session, ending the session with a lower ultrafiltration rate, plasma refill might be able to match the fluid removal rate (Kelly, 1996), and the blood pressure might be more stable (deVries et al., 1990). Clear benefit of ultrafiltration profiling in terms of published studies remains unclear (Parsons, Yuill, Llapitan, & Harris, 1997). Further developments led to the concept of modulating the sodium in the dialysate to reduce the potential complications associated with high sodium dialysate, while keeping the benefits of hemodynamic stability (Kelly, 1996; Palmer, 2001).
What is Sodium Profiling?
Sodium profiling is the means by which sodium in the dialysate fluid is manipulated in order to influence fluid shifts between the ICF and ECF, thus reducing or preventing the changes described earlier. Higher concentration of sodium in the dialysate fluid than in the plasma prevents reduction in ECF osmolality, preventing IC water absorption; it may also support plasma refilling (Bonomini et al., 1997; de Vries et al., 1991; Raja, 1996; Raja & Po, 1994; Stiller et al., 2001) (see Figure 1). During a routine dialysis session sodium is an easy variable to manipulate in order to control the ECF osmolality. Stiller et al. (2001) reported, however, that this increase in ECF volume may be minimal compared to the average blood volume depletion caused by ultrafiltration throughout the hemodialysis procedure.
Sodium profiling consists of changing the dialysate sodium (or conductivity) level from high to low or low to high in stepwise, linear or exponential fashion (see Figure 2). The effects of these profile types have been discussed in the literature, identifying differing effects on symptoms, vascular stability, and osmolality (Stiller et al., 2001). It is possible to see how stepwise sodium profiling delineates clear points at which sodium levels change and thus may ease data collection compared to a constantly changing sodium level seen with exponential and linear sodium profiling.
Current thinking concerning sodium profiling is aimed at modulation of the dialysate sodium over the course of the dialysis session, individually calculated according to a predetermined end sodium balance and the patient's own predialysis serum sodium (Bonomini, Coli, Feliciangeli, & Scolari, 1996; Di Guilio et al., 1998; Kelly, 1996; Ursino et al., 1997). Mathematical models have been formulated for this, similar to the urea kinetic model in use in many dialysis units today (Bonomini et al., 1996; Coli et al., 1997; Di Guilio et al., 1998; Flanigan, Khairullah, & Lim, 1997; Jenson, Dobbe, Squillace, & McCarthy, 1994; Pedrini, Ponti, Faranna,... |
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