Quenching the Thirst in Dialysis Patients

Dominic, Swapna; Ramachandran, S; Somiah, Surjit; Mani, Kevin; Dominic, S S

doi:10.1159/000189146

Cited by 41 publications

(4 citation statements)

References 10 publications

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“…The list of potential causative conditions is extensive: nausea and/or vomiting, 52 hemorrhage, 53 chronic renal failure, 44,54,55 heart failure, 11 fluid and electrolyte imbalances, 56 endocrine disorders, 57 end-stage disease, 58 and commonly used medications 59,60 (see Table for medications that may affect thirst in ICU patients).…”

Section: Identifying the Etiology Of Thirstmentioning

confidence: 99%

Thirst in Critically Ill Patients: From Physiology to Sensation

Arai

Stotts

Puntillo

2013

American Journal of Critical Care

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Critically ill patients often have distressful episodes of severe thirst, but the underlying complex biochemical, neurohormonal regulatory controls that regulate this primal sensation have rarely been addressed by clinicians. Subtle changes in plasma osmolality are the most potent stimulus for thirst. In response to increases in osmolality, osmoreceptors activate release of the neurohormone vasopressin (also known as antidiuretic hormone). The released vasopressin acts on the kidneys to conserve water to correct the hyperosmolar state. If this compensatory mechanism is unsuccessful, thirst arises to promote drinking. Thirst induced by marked volume loss, in contrast, is more closely related to the volemic and pressure changes regulated by the renin-angiotensin aldosterone system. Understanding the physiological mechanisms of thirst will help in understanding the pathophysiological consequences of underlying thirst-related disease and treatments in critically ill patients. Further clinical research is needed to elucidate the multiple inhibitory and excitatory neurohormonal stimuli that motivate patients’ intense desire for water.

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Section: Identifying the Etiology Of Thirstmentioning

confidence: 99%

Thirst in Critically Ill Patients: From Physiology to Sensation

Arai

Stotts

Puntillo

2013

American Journal of Critical Care

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“…But, on the other hand, aiming to reach eunatremia may increase the risk of intradialytic hypotension. Indeed, two studies reported a reduction in the frequency of intradialytic hypotension after decreasing dialysate sodium [ 9 , 18 ]. Therefore, individualization of dialysate sodium mainly influences the IDWG and leads to better BP control in patients with poorly controlled BP and this group of patients is generally asymptomatic.…”

Section: Discussionmentioning

confidence: 99%

Clinical Effects of Standard and Individualized Dialysate Sodium in Patients on Maintenance Hemodialysis

Eftimovska-Otovic¹,

Stojceva-Taneva²,

Grozdanovski³

et al. 2016

Open Access Maced J Med Sci

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BACKGROUND:The degree to which the dialysate prescription and, in particular, the dialysate sodium concentration influences blood pressure and interdialytic weight gain (IDWG) via changes in sodium flux, plasma volume or the other parameters is not well understood. The aim of the study was to investigate whether dialysis patients will have some beneficial effects of dialysate sodium set up according to serum sodium or sodium modeling.MATERIAL AND METHODS:Ninety-two nondiabetic subjects (52 men and 40 women) performed 12 consecutive hemodialysis (HD) sessions (4 weeks) with dialysate sodium concentration set up on 138 mmol/L (standard sodium – first phase), followed by 24 sessions (second phase) wherein dialysate sodium was set up according to individualized sodium. Variables of interest were: systolic, diastolic and mean blood pressure, pulse, IDWG, thirst score – (Xerostomia Inventory (XI) and Dialysis Thirst Inventory (DTI)) and side effects (occurrence of hypotension and muscle cramps). After the first phase, the subjects were divided into 3 groups: normotensive (N=76), hypertensive (N= 11) and hypotensive (N=5) based on the average pre-HD systolic BP during the whole period of the first phase.RESULTS:Sodium individualization resulted in significantly lower blood pressure (133.61 ± 11.88 versus 153.60 ± 14.26 mmHg; p=0.000) and IDWG (2.21 ± 0.93 versus 1.87 ± 0.92 kg; p=0.018) in hypertensive patients, whereas normotensive patients showed only significant decrease in IDWG (2.21 ± 0.72 versus 2.06 ± 0.65, p=0,004). Sodium profiling in hypotensive patients significantly increased IDWG (2.45 vs. 2.74, p= 0,006), and had no impact on blood pressure. Thirst score was significantly lower in normotensive patients with individualized-sodium HD and showed no change in the other two groups. During the second phase, hypotension occurred in only 1 case and muscle cramps in 10 normotensive patients.CONCLUSION:Individualized sodium resulted in clinical benefits in normotensive and hypertensive patients.

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“…Since excessive thirst and IWG is a common problem in chronic dialysis patients [15,16,17,18,19], we designed a study in order to search for an effective therapy to reduce fluid intake in those HD patients who had excessive weight gain between dialysis sessions (mean IWG was 2.6 kg in our study).…”

Section: Discussionmentioning

confidence: 99%

Influence of Dual Blockade of the Renin-Angiotensin System on Thirst in Hemodialysis Patients

Masajtis-Zagajewska

Nowicki²

2009

Nephron Clin Pract

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Background/Aims: Angiotensin II promotes sodium retention and influences the central regulation of fluid intake. Clinical studies on the effect of an angiotensin-converting enzyme inhibitor (ACEI) on xerostomia and thirst in chronic hemodialysis (HD) patients were scarce and gave contradictory results. We hypothesized that a more effective inhibition of the renin-angiotensin-aldosterone axis with the combined ACEI and angiotensin receptor antagonist administration may reduce thirst and xerostomia,thereby decreasing interdialytic weight gain (IWG) in HD patients. Methods: Twenty-one chronic HD patients (16 men, 5 women, mean age 54 ± 13 years, time on dialysis 50 ± 58 months) who had been on chronic ACEI therapy were studied. In a double-blind, crossover study, all subjects received in a random order either losartan (50 mg/day) or placebo for two 4-week periods with a 7-day wash-out. Basic biochemistry, serum electrolytes, plasma aldosterone, measurements of salivary flow rate after stimulation with paraffin chewing, and subjective xerostomia and thirst questionnaires were collected before dialysis sessions both before and after each treatment period. IWG and blood pressure were assessed at each dialysis. Results: The volume of saliva increased after losartan (from 1.2 ± 0.7 to 1.5 ± 1.0 ml/min, respectively; p = 0.03), but this was reflected neither by the severity of the symptoms of xerostomia assessed by the patients on a visual analog scale (31 ± 9 vs. 31 ± 8 mm, respectively) nor by the intensity of thirst (final score 22 ± 5 vs. 21 ± 5 at baseline). No changes of the mean IWG were observed during the treatment with losartan (2.5 ± 0.6 kg before and 2.4 ± 0.8 kg at the end of the treatment). Plasma aldosterone decreased at the end of the losartan therapy (from 151 ± 86 to 111 ± 51 pg/ml; p = 0.02). Predialysis serum potassium did not change during the study. Conclusions: The addition of an angiotensin receptor blocker to chronic ACEI therapy is not effective in reducing thirst and thereby IWG in chronic HD patients.

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Quenching the Thirst in Dialysis Patients

Cited by 41 publications

References 10 publications

Thirst in Critically Ill Patients: From Physiology to Sensation

Thirst in Critically Ill Patients: From Physiology to Sensation

Clinical Effects of Standard and Individualized Dialysate Sodium in Patients on Maintenance Hemodialysis

Influence of Dual Blockade of the Renin-Angiotensin System on Thirst in Hemodialysis Patients

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