Survival of Acute Hypernatremia Due to Massive Soy Sauce Ingestion

Carlberg, David; Borek, Heather A.; Syverud, Scott A.; Holstege, Christopher P.

doi:10.1016/j.jemermed.2012.11.109

Cited by 23 publications

(36 citation statements)

References 12 publications

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“…66 However, the fear of these complications, which have been reported only in young children, should not deter the aggressive rehydration of adults with acute hypernatremia to avoid brain hemorrhage or osmotic demyelination (Table 2). 76 In contrast to the risk of inadvertent overcorrection in patients with hyponatremia, there is little risk of inadvertent overcorrection in patients with hypernatremia, and adults with hypernatremia are often undertreated. 77,78 Conclusions Disorders of plasma sodium concentration expose cells to hypotonic or hypertonic stress.…”

Section: Limit Of Correction and Management Of Overcorrectionmentioning

confidence: 99%

Disorders of Plasma Sodium — Causes, Consequences, and Correction

2015

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T h e ne w e ngl a nd jou r na l o f m e dicine n engl j med 372;1 nejm.org January 1, 2015 55Review Article H uman cells dwell in salt water. Their well-being depends on the ability of the body to regulate the salinity of extracellular fluids. By controlling water intake and excretion, the osmoregulatory system normally prevents the plasma sodium concentration from straying outside its normal range (135 to 142 mmol per liter). Failure of the system to regulate within this range exposes cells to hypotonic or hypertonic stress. This review considers the causes and consequences of an abnormal plasma sodium concentration and offers a framework for correcting it. Pl a sm a Sodium Concentr ation a nd E x tr acellul a r T onicit yThe plasma sodium concentration affects cell volume. The term "tonicity" describes the effect of plasma on cells -hypotonicity makes cells swell and hypertonicity makes them shrink. Hypernatremia always indicates hypertonicity. Hyponatremia usually indicates hypotonicity, but there are exceptions (e.g., hyperglycemic hyponatremia and pseudohyponatremia) that are not covered in this review.Pl a sm a Sodium Concentr ation a nd the Elec troly te a nd Water Content of the Body Solute concentrations (osmolalities) must be equal inside and outside of cells because water channels (aquaporins) make cell membranes permeable to water. 1,2The "sodium pump" (Na + /K + -ATPase) functionally excludes sodium from cells, exchanging it for potassium by means of active transport. Although sodium is largely extracellular and potassium is intracellular, body fluids can be considered as being in a single "tub" containing sodium, potassium, and water, because osmotic gradients are quickly abolished by water movement across cell membranes. As such, the concentration of sodium in plasma water should equal the concentration of sodium plus potassium in total body water. This theoretical relationship was validated empirically by Edelman et al., 3 who used isotopes to measure exchangeable body cations and water. Edelman and colleagues described the relation between these variables with the following equation: −25.6, (Na + e + K + e ) total body H 2 O [Na + ] in plasma H 2 O=1.11 ×where Na + e is exchangeable sodium, K + e exchangeable potassium, and H 2 0 water. This equation has an intercept (−25.6); the regression line relating plasma sodium

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Section: Limit Of Correction and Management Of Overcorrectionmentioning

confidence: 99%

Disorders of Plasma Sodium — Causes, Consequences, and Correction

2015

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“…The results are consistent with our previous report, in which we adjusted for the serum sodium and the hypernatremia relapse and excluded patients with an RRSeNa ≤ 0.5 mEq/L/h. However, only a few case reports have suggested that excessive correction is not associated with poor outcomes (28,29). Carlberg DJ described that the case of a 19-year old man whose peak serum sodium was 196 mEq/L and who experienced a reduction rate of serum sodium of 1.7mEq/L/h (28).…”

Section: Discussionmentioning

confidence: 99%

“…However, only a few case reports have suggested that excessive correction is not associated with poor outcomes (28,29). Carlberg DJ described that the case of a 19-year old man whose peak serum sodium was 196 mEq/L and who experienced a reduction rate of serum sodium of 1.7mEq/L/h (28). The patient survived with no neurologic deficits.…”

Section: Discussionmentioning

confidence: 99%

The Reduction Rate of Serum Sodium and Mortality in Patients Undergoing Continuous Venovenous Hemofiltration for Acute Severe Hypernatremia

Liu

Bai

et al. 2016

The American Journal of the Medical Sciences

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“…Isolated increase in body sodium may occur as a result of intake of salt tablets or infusion of hypertonic solutions of sodium salts. Salt poisoning from near-drowning in sea water[35], during environmental disasters or after suicidal attempts with soy sauce ingestion[36] have also been reported.…”

Section: Hypernatremiamentioning

confidence: 99%

Hypertonicity: Clinical entities, manifestations and treatment

Rondon‐Berrios

Argyropoulos

Ing

et al. 2017

WJN

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Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperglycemia. Hypernatremia results from relative excess of body sodium over body water. Loss of water in excess of intake, gain of sodium salts in excess of losses or a combination of the two are the main mechanisms of hypernatremia. Hypernatremia can be hypervolemic, euvolemic or hypovolemic. The management of hypernatremia addresses both a quantitative replacement of water and, if present, sodium deficit, and correction of the underlying pathophysiologic process that led to hypernatremia. Hypertonicity in hyperglycemia has two components, solute gain secondary to glucose accumulation in the extracellular compartment and water loss through hyperglycemic osmotic diuresis in excess of the losses of sodium and potassium. Differentiating between these two components of hypertonicity has major therapeutic implications because the first component will be reversed simply by normalization of serum glucose concentration while the second component will require hypotonic fluid replacement. An estimate of the magnitude of the relative water deficit secondary to osmotic diuresis is obtained by the corrected sodium concentration, which represents a calculated value of the serum sodium concentration that would result from reduction of the serum glucose concentration to a normal level.

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Survival of Acute Hypernatremia Due to Massive Soy Sauce Ingestion

Cited by 23 publications

References 12 publications

Disorders of Plasma Sodium — Causes, Consequences, and Correction

Disorders of Plasma Sodium — Causes, Consequences, and Correction

The Reduction Rate of Serum Sodium and Mortality in Patients Undergoing Continuous Venovenous Hemofiltration for Acute Severe Hypernatremia

Hypertonicity: Clinical entities, manifestations and treatment

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