Postoperative Hyponatremia despite Near-Isotonic Saline Infusion: A Phenomenon of Desalination

Steele, A.

doi:10.7326/0003-4819-126-1-199701010-00003

Cited by 242 publications

(134 citation statements)

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“…Fluid intake should also be monitored to avoid congestive heart failure. In the rare patient with SIADH or RSW, the desalinization syndrome can be observed when the administration of isotonic saline exacerbates the hyponatremia (31). This occurs when the total UNa and UK exceed 150 mmol/L, in which case hypertonic saline and water restriction should be instituted.…”

Section: Discussionmentioning

confidence: 99%

More on Renal Salt Wasting Without Cerebral Disease

Bitew

Imbriano

Miyawaki

et al. 2009

Clinical Journal of the American Society of Nephrology

116

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Background and objectives: The existence and prevalence of cerebral salt wasting (CSW) or the preferred term, renal salt wasting (RSW), and its differentiation from syndrome of inappropriate antidiuretic hormone (SIADH) have been controversial. This controversy stems from overlapping clinical and laboratory findings and an inability to assess the volume status of these patients. The authors report another case of RSW without clinical cerebral disease and contrast it to SIADH. Design, setting, participants, & measurements: Three patients with hyponatremia, hypouricemia, increased fractional excretion (FE) of urate, urine sodium >20 mmol/L, and concentrated urines were infused with isotonic saline after collection of baseline data.Results: One patient with RSW had pneumonia without cerebral disease and showed increased plasma aldosterone and FEphosphate, and two patients with SIADH had increased blood volume, low plasma renin and aldosterone, and normal FEphosphate. The patient with RSW responded to isotonic saline by excretion of dilute urines, prompt correction of hyponatremia, and normal water loading test after volume repletion. Hypouricemia and increased FEurate persisted after correction of hyponatremia. Two patients with SIADH failed to dilute their urines and remained hyponatremic during 48 and 110 h of saline infusion.Conclusions: The authors demonstrate appropriate stimulation of ADH in RSW. Differences in plasma renin and aldosterone levels and FEphosphate can differentiate RSW from SIADH, as will persistent hypouricemia and increased FEurate after correction of hyponatremia in RSW. FEphosphate was the only contrasting variable at baseline. The authors suggest an approach to treat the hyponatremic patient meeting criteria for SIADH and RSW and changing CSW to the more appropriate term, RSW.

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Section: Discussionmentioning

confidence: 99%

More on Renal Salt Wasting Without Cerebral Disease

Bitew

Imbriano

Miyawaki

et al. 2009

Clinical Journal of the American Society of Nephrology

116

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“…The higher excretion of salt in these patients could result from expansion of the extracellular compartment, which is a powerful stimulus for the renal excretion of sodium. (15,16) The use of restrictive or liberal fluid therapy in the intraoperative period remains as a controversial issue. In contrast, after the surgery, ongoing evidence favors fluid restriction.…”

Section: Discussionmentioning

confidence: 99%

Fluidos no período pós-operatório: efeitos da falta de ajuste ao peso corpóreo

Vázquez¹,

Masevicius²,

R³

et al. 2011

Rev. bras. ter. intensiva

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Objective: To compare the differences in fluid and electrolyte balance in patients with low and high weight in the first postoperative day.Methods: Over a period of 18 months, we prospectively evaluated 150 patients in the first 24 hours after surgery, in a university-affiliated hospital intensive care unit. Patients with low weight (≤ 60 kg) and high body weight (≥ 90 Kg) were compared in terms of fluid intake and output.Results: No significant differences were observed in the volume (4334 ± 1097 vs. 4644 ± 1957 ml/24 h) and composition of the fluids administered (481 ± 187 vs. 586 ± 288 mEq [Na + ] administered /24 h). The 24 h urine output was similar (2474 ± 1597 vs.2208 ± 678 ml/24 h) but low weight group showed higher electrolyte elimination (296 ± 195 vs.192 ± 117 mEq [Na + ] urine /24 h, p = 0.0246). When the administered fluids were adjusted for body weight, the volume and amount of electrolytes of fluids administered were higher in the low weight group (79 ± 21 vs. 47 ± 22 ml/kg/24 h, p<0.0001 and 8.8 ± 3.4 vs. 5.8 ± 3.3 mEq [Na + ] administered / kg/24 h, p=0.017, respectively). This group also showed higher urine output and electrolyte elimination (45 ± 28 vs. 22 ± 7 ml/kg/24 h, p = 0.0002 and 5.3 ± 3.5 vs. 1.8 ± 1.2 mEq [Na + ] urine /kg/24 h, p<0.0001, respectively).Conclusions: The lack of adjustment of the fluid therapy to body weight determined that low weight patients received more fluid than high weight patients according to their body weight. This fluid overload could be compensated by increased urine output and electrolyte elimination.

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“…It is possible that she had cerebral salt wasting, even though the diagnosis cannot be confirmed until the patient has a contracted ECF volume (15). In addition, "desalination" of several of the liters of isotonic saline that was administered in the perioperative period could play a role (16). While Na ϩ is being excreted, the medullary tonicity rises because dDAVP was administered (urine [Na ϩ ] rose to 300 mM).…”

Section: Efw Tonicitymentioning

confidence: 99%

The Nephrology Quiz and Questionnaire

Narins¹,

Halperin²,

Danovitch³

et al. 2006

Clinical Journal of the American Society of Nephrology

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T he Nephrology Quiz and Questionnaire (NQQ) continues to be the most popular of the 2-hr Clinical Nephrology Conferences held at our annual Renal Week. Our faculty presented eight puzzling cases that prompted some lively discussions at the recent Philadelphia meeting.As most of you know, each of the four faculty is charged with developing two cases, each of which involve some controversial aspect of diagnosis, management, or pathophysiology related to a renal or an electrolyte disorder. One or two questions follow each case. Before Renal Week, we e-mail these cases and multiple-choice questions to all our members and ask them to send us their answers. At the meeting, the collated answers to each question are presented by the faculty, and they discuss their "correct" answer to each question. The responses from the Nephrology Training Program Directors and those from all other nephrologists are assessed and presented separately. In years past, we have e-mailed the answers to the membership after the Renal Week meeting. CJASN will now be the new home for the discussions of NQQ cases. We hope that this "distillate from Philadelphia" will serve as a good review for those of you who were at the session and will provide fresh insights for those of you who missed the Clinical Nephrology Conferences. Case 1: Mitchell L. Halperin (NQQ Presenter), Kamel S. Kamel, and Desmond BohnTwo days ago, a 24-yr-old, healthy, 50-kg man developed profuse diarrhea ("rice water" consistency) after drinking contaminated water. On physical examination, he appeared very ill and cyanotic. His BP was 90/60 mmHg, his heart rate was 110 beats/min, and his jugular venous column height was below the sternal angle. The remainder of the examination was not relevant.Laboratory studies on admission included serum electrolytes (in mM) Na 140, HCO 3 24, K 4.6, Cl 95; pH 7.39, Pco 2 (arterial) 39 mmHg, glucose 72 mg/dl (4.0 mM), creatinine 3.0 mg/dl (345 M), total protein 132 g/L (13.2 g/dl), and hematocrit 60%. On day 1, the volume of his diarrhea was approximately 5 L and contained (in mM) 140 Na, 15 K, 115 Cl, and 40 HCO 3 . (Figures 1 and 2). Question 1A: d. Metabolic acidosis and metabolic alkalosis Question 1B: a. Yes Question 1A Discussion of Case 1Ingestion of water heavily contaminated with the vibrio cholera bacillus causes the abrupt onset of massive diarrhea. Stool volume is often approximately 5 L/d and contains approximately 40 mM HCO 3 Ϫ (1). These massive and acute losses of alkali dwarf its potential replacement by ingestion (limited in these sick patients), generation by gastric HCl loss, or renal new HCO 3 Ϫ formation linked to the urinary excretion of NH 4 ϩ (2).Predictably, these patients should develop a metabolic acidosis. Notwithstanding, our patient (and many others like him [1]) has normal arterial pH, Pco 2 and plasma HCO 3 Ϫ concentration (P HCO3 ). Question 1A. From analysis of the laboratory data, either the patient does not have a metabolic acid-base disorder because the arterial pH (7.39) and P HCO3 (24 mM) are in the n...

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Postoperative Hyponatremia despite Near-Isotonic Saline Infusion: A Phenomenon of Desalination

Cited by 242 publications

References 0 publications

More on Renal Salt Wasting Without Cerebral Disease

More on Renal Salt Wasting Without Cerebral Disease

Fluidos no período pós-operatório: efeitos da falta de ajuste ao peso corpóreo

The Nephrology Quiz and Questionnaire

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