Fluid Overload: 164 (Contributions to Nephrology)


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Contributions to Nephrology

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Management of the Fluid Overloaded Patient

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Welcome back. Just a moment while we sign you in to your Goodreads account. There is no doubt that fluid intake is the most important determinant of weight gain between one session of haemodialysis and the next, particularly in patients with minimal residual urine output. In patients with normal bowel function, the amount of water lost in the stools is small. However, it is arguable that fluid intake is determined, in turn, by sodium chloride intake.

This lack of a relationship is less surprising than it seems, because it is the change in plasma volume, not in total extracellular volume or total body water, which is likely to result in acute changes in blood pressure during fluid removal [ 15 ]. The distribution of extra water ingested in a dialysis patient depends on the amount of salt—sodium chloride—that is ingested with it.

Think what happens to the serum sodium concentration of a typical dialysis patient.

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Impact of Systemic Volume Status on Cardiac Magnetic Resonance T1 Mapping

One study using this technique showed that fluid gained between dialysis sessions largely remains in the extracellular space [ 17 ]. The only possible reason for this is that the extra fluid is held in the extracellular space by extra sodium, ingested during dialyses. It is very difficult indeed for a conscious patient to ignore thirst, and severe thirst will drive a patient to find fluid wherever they can—for example, drinking the water from the flower vase.

Using hypertonic saline infusions, Argent et al. It follows that no dialysis patient whose sodium intake exceeds sodium output will be able to resist the stimulus to drink to maintain serum osmolality within the normal range, unless first rendered unconscious! We should concentrate on advising and helping dialysis patients to limit their salt intake, which will help limit thirst.

Advising dialysis patients to restrict fluid intake when they have not had advice on how to limit their salt intake is inhumane, because they are being made to feel guilty and inadequate at being unable to restrict their fluid intake—and is a waste of time. Hypovolaemia can also stimulate thirst, of course, so inappropriately low target weights might cause thirst as well as increased appetite for salt. This is probably less much common as a cause for thirst than salt overload.

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Regression of left ventricular hypertrophy has also been reported [ 26 ]. Such a policy would reduce unnecessary thirst, weight gain, and hypertension caused by dialysing sodium into patients. In peritoneal dialysis too, low sodium dialysate results in reduction in blood pressure [ 28 ]. Sodium profiling during dialysis has been promoted as a way of improving cardiovascular stability during dialysis without causing net sodium gain.

However, this assumption has never been tested adequately. It is quite possible, for instance, that high extracellular fluid sodium concentration results in flux of water from cells.

This results in intracellular dehydration, which might then cause rebound hypernatraemia after completion of dialysis, which might explain why some sodium profiled patients appear to become more thirsty, resulting in a vicious cycle of increasing fluid gains and increasing symptoms during rapid volume removal on dialysis. One of the intriguing observations in patients undergoing long slow dialysis at Tassin, where blood pressure is nearly universally controlled with salt restriction and fluid removal on dialysis [ 30 ], is that compared with patients undergoing standard dialysis, peripheral vascular resistance is low—whereas one might expect a higher peripheral vascular resistance as a result of vasoconstriction in response to relative extracellular volume depletion [ 31 ].

The cause of this paradoxical vasodilatation is not certain. It may relate to a more efficient removal during long slow dialysis of vasconstrictor substances, although these have not been identified. Water ingested without sodium will distribute throughout total body water, and will, therefore, have much less impact on extracellular volume.

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The water load would cause a small drop in extracellular sodium concentration. This would result in a greater osmotic gradient between dialysate and plasma during dialysis, favouring rapid removal of the extra water. Theoretically, a high water load could result in hyponatraemia, and the increased cell volume caused by water entering cells could cause cerebral oedema. Some advice to avoid excessive water intake would, therefore, remain necessary. One small prospective randomized controlled trial has examined this strategy: 28 haemodialysis patients were randomized to very low sodium intake, with advice to drink only when thirsty, or to standard diet and fluid intake.

During the low sodium diet, weight gains were significantly lower, despite free fluid intake, than on the standard diet [ 34 ]. The drawback to this argument is the practical difficulty of persuading patients to limit dietary sodium intake. The high sodium content of many processed foods means that simply avoiding extra salt at the table and in cooking will not be enough to reproduce the effects of tight dietary sodium intake described in this article. However, any reduction in salt intake is likely to have a beneficial effect in the right direction.

Look after the salt intake, and the water will look after itself. Most dialysis patients want to stay alive, and will, within reason, do what is asked of them. Asking patients with severe thirst to drink less than 1 l a day is illogical, inhumane, and should become part of the history of dialysis in the twentieth century. Correspondence and offprint requests to : C. A preliminary version of this paper appeared on the website www. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.

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Close mobile search navigation Article Navigation. Volume Article Contents. The relationship between water intake and ECF volume depends on sodium intake. Where does the extra fluid accumulate in haemodialysis patients? What governs fluid intake in dialysis patients? What is the impact of dialysate sodium? How else may sodium overload influence blood pressure?

Where is the catch? Advising dialysis patients to restrict fluid intake without restricting sodium intake is not based on evidence and is a waste of time Charles R. Oxford Academic. Google Scholar. Cite Citation. Permissions Icon Permissions.

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Introduction Advice on the restriction of fluid intake is a cornerstone of management of patients with kidney failure. Two things follow from this simple argument. Conclusions Look after the salt intake, and the water will look after itself. Dialysis and processed foods are the main sources of salt excess. Low weight gains should cause more alarm than high weight gains.

Zaccaria Ricci

Weight gain between dialyses bears little relationship to plasma volume or to blood pressure. Current status of renal replacement therapy in Japan. Am J Kidney Dis. Interdialytic weight gain and nutritional parameters in chronic hemodialysis patients.

Fluid Overload: 164 (Contributions to Nephrology) Fluid Overload: 164 (Contributions to Nephrology)
Fluid Overload: 164 (Contributions to Nephrology) Fluid Overload: 164 (Contributions to Nephrology)
Fluid Overload: 164 (Contributions to Nephrology) Fluid Overload: 164 (Contributions to Nephrology)
Fluid Overload: 164 (Contributions to Nephrology) Fluid Overload: 164 (Contributions to Nephrology)
Fluid Overload: 164 (Contributions to Nephrology) Fluid Overload: 164 (Contributions to Nephrology)

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