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Part 4: Technical Advances in PD |
Renal Unit, Leeds General Infirmary, United Kingdom
Correspondence to: G. Woodrow, Renal Unit, Leeds General Infirmary, Great George Street, Leeds LS1 3EX U.K. graham.woodrow{at}leedsth.nhs.uk
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ABSTRACT |
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 TOP ABSTRACT DISCUSSIONCONCLUSIONSREFERENCES |
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Loss of sodium and water excretion with disruption of volume homeostasis
is a crucial abnormality of end-stage renal failure. Fluid management is a
fundamental function of dialysis therapy, but studies show frequent occult
fluid overload, hypertension, and cardiac dysfunction in peritoneal dialysis.
A rigorous approach to fluid management in PD can achieve excellent fluid,
hypertension, and cardiovascular results in clinical practice. The present
article explores the reasons for fluid overload and poor ultrafiltration in
peritoneal dialysis patients and discusses optimal assessment and management
of these problems.
KEY WORDS: Fluid balance; ultrafiltration; bioelectrical impedance; peritoneal membrane function.
Loss of sodium and water excretion with disruption of volume homeostasis is a crucial abnormality of end-stage renal failure. In peritoneal dialysis (PD), correction of this situation is attempted by dialysis prescription to optimize sodium and water removal, administration of diuretics to enhance residual urine output, and placement of limits on sodium and water intake.
Fluid management is a fundamental function of dialysis therapy. However, evidence suggests that hydration in PD is frequently not normalized. Symptomatic fluid retention is common in PD patients (1). Fluid overload is an important cause of hypertension in dialysis patients (2), and studies show frequent occult fluid overload, hypertension, and cardiac dysfunction in PD (3–6), which may deteriorate with time, perhaps as residual renal function is lost (7,8).
Evidence for the association of water and salt removal with patient outcomes is increasing (9,10), and ultrafiltration failure is an important cause of PD technique failure. However, evidence shows that a rigorous approach to fluid management in PD, even with standard therapies, can achieve excellent fluid, hypertension, and cardiovascular results in clinical practice (11,12).
A clinical approach of limiting sodium and fluid intake and appropriately adjusting the dialysis prescription to achieve adequate ultrafiltration can achieve excellent blood pressure control (without antihypertensive drugs in most patients) and can encourage maintenance of good cardiac function and low prevalence of left ventricular hypertrophy (11,12). Automated PD provides an additional option for managing ultrafiltration problems in high transporters (though perhaps at the price of less good sodium removal because of sodium sieving), and increasingly impressive evidence is highlighting the benefits of icodextrin in improving management of the long dwell in PD, with enhanced fluid and sodium removal; beneficial effects on blood pressure (13), patient hydration status, and cardiac function (14,15); and concomitant improvement in the biocompatibility and metabolic aspects of PD.
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DISCUSSION |
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TOPABSTRACTDISCUSSIONCONCLUSIONSREFERENCES |
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A thorough and systematic approach to fluid management is important. The first stage is regular assessment of fluid balance and identification of the presence of fluid abnormalities. When fluid excess has been diagnosed, the patient should be evaluated for the presence of reversible factors such as excess sodium and water intake, the appropriateness of the dialysis prescription to the patient, and mechanical factors such as drainage problems and dialysate leaks. Once these factors have been excluded, assessment of the peritoneal membrane can objectively determine the presence of ultrafiltration failure because of membrane dysfunction and can provide additional information about peritoneal transport status that will guide further management (16).
MONITORING HYDRATION
Although much emphasis has been placed on membrane function and
ultrafiltration management, a crucial area in need of greater attention is the
monitoring of hydration and the initial diagnosis of fluid balance problems in
PD patients.
In healthy individuals, complex homeostatic mechanisms continuously detect changes in fluid status and appropriate adjustments then keep intravascular volume regulated within tight physiologic parameters. In contrast, in the PD patient, practitioners rely at best on daily observation by the patient of weight, fluid removal, and blood pressure, and on far less frequent assessments by the medical, nursing, and dietetic staff. To optimize fluid-related outcomes in PD, reliable and prompt detection of abnormalities in fluid balance are essential to enable the appropriate therapeutic changes. It may be that, at the current state of PD development, with the tools at our disposal, the crucial barrier to improving fluid management is not a lack of strategies to enhance fluid removal, but the existence of limitations to identifying when they should be employed.
Daily weighing by patients is a routine part of PD management, and weighing is valuable in detecting changes in body fluid content. However, day-to-day variability in weight occurs in normal individuals. Also, malnutrition is a common and serious complication of PD patients. Thus, by maintaining a stable body weight as dialysis prescription and intake are adjusted, a PD patient developing protein–calorie malnutrition over time may progressively acquire extracellular fluid retention that balances loss of body cell mass (BCM) or fat mass (or both) and that fails to become clinically apparent until fluid excess is quite marked. The result is a serious situation of simultaneous malnutrition and complications of fluid overload. Thus, regular monitoring and objective assessment of hydration (and nutrition) is essential in PD. But how should this goal be accomplished?
Routine physical examination provides a useful, but imprecise picture of fluid status. Assessment may be complicated when cardiovascular disease leads to disturbance of fluid distribution in the body. Thorough examination involves assessment of a composite of various aspects of hydration and cardiovascular function. Significant fluid overload may exist in the absence of any typical signs of fluid retention.
Often, hypertension may be the only feature of fluid excess, and the presence of hypertension should usually be addressed by attention to removing any fluid excess before utilizing antihypertensive agents. Other clinical features of fluid retention include peripheral edema, elevated jugular venous pressure, and signs of pulmonary venous congestion or pulmonary edema (although absence of these conditions does not exclude fluid excess). Postural hypotension in the absence of autonomic neuropathy—for example, diabetes—or excess antihypertensive treatment, is a sensitive measure of fluid depletion.
"Dry" or "target" body weight is variously defined as "edema-free weight" (which does not necessarily exclude the presence of fluid excess) or minimal weight on progressive fluid depletion tolerated without adverse effects. The practice in hemodialysis of gradually drying a patient out until hypotension or symptoms of hypovolemia occur is less easy to apply in PD patients, because aggressive fluid removal is less easily achieved in PD than in hemodialysis. However, with care, the steady state of PD provides advantages in determining dry weight through response to weight reduction by gradual removal of fluid. Unlike the case in hemodialysis, rapid fluid removal causing hypotension, despite the presence of overall fluid excess, is not a problem in PD. Furthermore, PD does not have the same fluctuation between states of fluid excess and of possible dehydration. Also, excess fluid removal, with risk of loss of residual renal function, is not necessarily desirable.
MEASURING HYDRATION
More sensitive and objective measures of hydration are needed. Chest X-ray
may show pulmonary venous congestion, and cardiac diameter is of value in
monitoring changes over a longer time course
(12), but these approaches are
not practical enough for shorter-term monitoring. Other techniques
investigated include bioelectrical impedance (BIA), ultrasound measurement of
inferior vena cava (IVC) diameter, and measurement of serum natriuretic
peptide concentration.
Bioelectrical Impedance: The most extensively studied technique is BIA, and it is the most promising for routine monitoring of fluid status and nutrition in PD patients. It involves measurement of the body's impedance to passage of a small alternating electrical current. A variety of technologies and ways of analyzing the data are available, and so to interpret the results produced and to appreciate the limitations of the data, an understanding of how the individual systems work is important (17).
Electrical current is conducted by body water, the major component of lean (fat-free) tissue. Fat acts as an electrical insulator. Simple single-frequency BIA assumes that impedance is inversely related to total body water (TBW), which is estimated from predictive equations incorporating terms for impedance, height and weight, and sex (18). However, TBW comprises both extracellular water (ECW), which reflects hydration, and intracellular water (ICW), which reflects BCM (and thus nutrition and wasting rather than hydration). Thus, for BIA to be of value in assessing hydration, further developments were needed to allow ECW and ICW—that is, hydration and nutritional change—to be distinguished.
Impedance of the body to an electrical current consists of a major resistance component (R) and a smaller reactance component (Xc) attributable to a capacitance effect of cell membranes. Cell membranes limit the passage of current into the ICW space to a degree that varies with the frequency of the current. At low frequency, current passes through ECW; with increasing frequency, penetration of the ICW space increases.
An approach used in some commercially produced analyzers is bioimpedance spectroscopy (19). This technique involves measurements at a large number of frequencies, with mathematical modeling of the data to estimate the theoretic resistance at a frequency of zero (where current would be entirely restricted to ECW) and at infinite frequency (where current would freely pass through the entire TBW space). Analysis thus allows for estimation of separate values for ECW, ICW, and TBW, with ECW being the marker of hydration.
With BIA, ECW is often normalized to the individual patient by expression as a ratio—ECW/ICW or ECW/TBW— measuring hydration. One strategy for using BIA in the clinical setting is to plot ECW/TBW ratios on a graph against age (because the ratio varies with age), and comparing the curve with the 95% confidence limits for healthy individuals. Early experience showed that this approach could be effectively used by nursing staff to incorporate BIA into clinical practice (20).
However, the range of normality is sufficiently large that precisely determining normal hydration is not possible. Also, even if the "normal" ECW volume could be determined, the "ideal" hydration state in a PD patient may be different because of the presence of cardiovascular disease (needing either a higher ECW to avoid hypotension or a lower volume in a patient prone to pulmonary edema). Also, the denominator of these ratios contains ICW, which reflects BCM (and thus nutritional state), and so the ratio also inversely reflects nutritional state or BCM loss (common in renal disease) in addition to hydration (21). As a measure of hydration, ECW may be better when normalized to another index of individual patient size, such as body height (21).
An alternative approach is to use single-frequency BIA, with separate analysis of the magnitude of resistance and reactance, and of the relationship between them (phase angle), which reflects the ratio of ECW and ICW. These data can be plotted graphically ("R/Xc graph"), where regions representing the area within the 95% confidence limits of the normal population can be determined, and changes in two dimensions represent relative changes of ECW and ICW (22). Phase angle itself is certainly important as a reflection of a composite of hydration and nutritional state, and it predicts outcome in PD patients (23).
Inferior Vena Cava Diameter: Ultrasound can measure IVC diameter and "collapsibility" with respiration, which have been shown to reflect the hydration state in dialysis patients (24). However, the technique does not yet seem to have developed to a point where it has proved to be of value in routine clinical practice. A study of the ability of methods including BIA, IVC ultrasound, and blood volume monitoring techniques in hemodialysis patients showed that only BIA demonstrated sufficient sensitivity to reliably detect important changes in ECW volume (25).
Natriuretic Peptides: Natriuretic peptides have been proposed as a marker of hydration status, and importantly, one that would specifically reflect intravascular volume. However concentrations in blood are also affected by renal failure and, importantly, are altered by cardiac dysfunction, and so they are not at present useful as pure markers of hydration (26).
ADDRESSING THE REVERSIBLE CAUSES OF FLUID OVERLOAD
Having identified the presence of fluid retention in a PD patient, the next
step is careful evaluation for reversible causes.
Identification of excess fluid intake is important, and factors such as a need for patient education or an excess intake of sodium or the presence of hyperglycemia as causes of excess thirst should be sought.
Measurement of urine output will determine if loss of residual renal function in the otherwise stable patient is the cause of fluid accumulation.
Measurement of ultrafiltration will determine if inadequate fluid removal is the cause. It is important that the patient on continuous ambulatory peritoneal dialysis (CAPD) be aware that bags are "overfilled" beyond their designated volume to provide fluid for the "flush" element of the exchange, and if that overfill volume is not accounted for and the infused volume is taken as stated on the bag, ultrafiltration may be significantly overestimated (27). Where fluid removal is poor, the patient should also be assessed for fluid leaks and mechanical drainage problems.
The dialysis prescription should be assessed to ensure that it is appropriate to the individual patient. The most common problem is the long dwell, whose duration allows glucose absorption and subsequent loss of osmotic effect, with reduced or negative ultrafiltration. A golden rule of PD prescription is to avoid negative ultrafiltration dwells. Where negative ultrafiltration occurs in the long dwell, it can be addressed by the use of more hypertonic glucose or of icodextrin, or by performing an extra dwell (day dwell in automated PD or automated night exchange in CAPD) to shorten dwell times. If poor ultrafiltration from short dwells occurs, attention should be paid to dwell length and the tonicity of glucose dialysate. An important mistake is the use of inadequate glucose concentrations out of concern about metabolic and biocompatibility effects. We should not accept fluid overload as the price of reducing dialysate glucose in clinical management.
A more formal assessment of peritoneal membrane function will allow determination of membrane transport status, which can aid in logical prescription changes and can confirm or refute the presence of an intrinsic membrane problem or ultrafiltration failure. The peritoneal equilibration test (PET) is the most familiar, consisting of a 4-hour dwell of 2.27% glucose dialysate, with analysis of dialysate-to-plasma creatinine and initial-to-final dialysate glucose concentration, determining transport status (28). In addition, a net ultrafiltration volume of less than 100 mL defines ultrafiltration failure.
The alternative is the modified PET, which uses 3.86% glucose dialysate (16,29). In that test, an ultrafiltration volume of less than 400 mL defines ultrafiltration failure. The modified PET is a more reliable measure than the standard PET in diagnosing the presence of ultrafiltration failure. In addition, it allows for assessment of the phenomenon of sodium sieving, which provides further information regarding membrane function, including water transport across endothelial aquaporin water channels.
Where the PET or modified PET shows ultrafiltration above threshold, the patient should be assumed not to have membrane failure and should be reassessed for reversible causes of fluid retention. If ultrafiltration failure is confirmed, transport status will aid in diagnosing the mechanism and choosing appropriate management. The commonest cause is high transport status, which may be inherent from the start of PD, acquired over time on PD with exposure to dialysate and with the effects of peritonitis and of uremia itself, or a temporary effect following peritonitis.
The presence of both poor ultrafiltration and low transport status is rare. It suggests major disruption of the peritoneal space, resulting in the serious combination of poor clearance and poor fluid management, which may require transfer to hemodialysis. However, a catch is that this finding may represent the combination of low transport status with poor drainage, potentially because of a reversible mechanical problem or a leak that should first be excluded. Low ultrafiltration with high-average or low-average transport status may result from situations of enhanced abdominal fluid reabsorption, aquaporin deficiency, or again, the coincidental presence of mechanical or leakage problems.
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CONCLUSIONS |
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TOPABSTRACTDISCUSSIONCONCLUSIONSREFERENCES |
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TOPABSTRACTDISCUSSIONCONCLUSIONSREFERENCES |
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This article has been cited by other articles:
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  A Power, N Duncan, and C Goodlad Management of the dialysis patient for the hospital physician Postgrad. Med. J., July 1, 2009; 85(1005): 376 - 381. [Abstract] [Full Text] [PDF]
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| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
