About all

Dehydration hyponatremia: Hyponatremia (Low Sodium) Signs & Symptoms, Treatment, Causes

a simple approach to hyponatremia

CMAJ. 2004 Feb 3; 170(3): 365–369.

From the Department of Medicine, Division of Nephrology, Queen’s University, Kingston, Ont. (all authors)

Copyright © 2004 Canadian Medical Association or its licensorsThis article has been cited by other articles in PMC.

Abstract

HYPONATREMIA IS COMMON IN BOTH INPATIENTS and outpatients. Medications are often the cause of acute or chronic hyponatremia. Measuring the serum osmolality, urine sodium concentration and urine osmolality will help differentiate among the possible causes. Hyponatremia in the physical states of extracellular fluid (ECF) volume contraction and expansion can be easy to diagnose but often proves difficult to manage. In patients with these states or with normal or near-normal ECF volume, the syndrome of inappropriate secretion of antidiuretic hormone is a diagnosis of exclusion, requiring a thorough search for all other possible causes. Hyponatremia should be corrected at a rate similar to that at which it developed. When symptoms are mild, hyponatremia should be managed conservatively, with therapy aimed at removing the offending cause. When symptoms are severe, therapy should be aimed at more aggressive correction of the serum sodium concentration, typically with intravenous therapy in the inpatient setting.

Case

A 72-year-old woman presents to your office with a 2-day history of presyncope when rising from a chair. She has been taking hydrochlorothiazide, 25 mg/d, for 5 years for systolic hypertension. Over the last week she has had a bout of viral gastroenteritis with marked diarrhea. She has been trying to replace the lost fluids by drinking 2–3 L of water per day. You determine that when she rises from a seated position, her blood pressure drops 20 mm Hg; her jugular venous pressure is low. Serum levels are as follows: sodium 128 mmol/L, potassium 3.1 mmol/L, creatinine 125 mmol/L and urea nitrogen 10 mmol/L.

What is your approach to this woman’s hyponatremia?

Hyponatremia is common in both inpatients and outpatients. Its causes are numerous and often elusive. Having a simple approach to assessment and treatment can be helpful in most cases that present in clinical practice. This review is meant to be a simplified, clinically based overview of the diagnosis and management of hyponatremia. Pathophysiological details of common and rare causes of hyponatremia and a detailed laboratory approach to diagnosis can be found elsewhere.1

Diagnosis

The symptoms and signs of hyponatremia vary from subtle to extreme; none is specific (). The diagnosis is confirmed by laboratory findings. Hyponatremia is typically defined as a serum sodium concentration of less than 134 mmol/L. In the past, hyponatremia was often diagnosed erroneously when the patient had high levels of serum lipids or plasma proteins. This should no longer be a concern because of the sodium electrode method used in almost every centre in Canada. In addition, hyponatremia occurs, but is not usually symptomatic, when the serum osmolality is elevated by severe hyperglycemia or mannitol infusion. The lowered serum sodium concentration is due to dilution by osmotic shifts of water out of cells. In these cases, the high serum osmolality will help to differentiate these causes from other “true” causes.

“True” hyponatremia occurs when the serum osmolality or tonicity is decreased. For this defect to occur, there has to be some inability of the body to excrete free water through the kidneys despite continued water intake. This can occur in the following 3 settings ().

Contracted extracellular fluid (ECF) volume

With ECF volume contraction from any cause (diarrhea, vomiting, excessive sweating, diuretic use), the release of antidiuretic hormone (ADH) is stimulated to defend ECF volume; this makes the kidney’s distal tubules more permeable to water reabsorption. Furthermore, renin is released in response to the decreased renal perfusion secondary to ongoing volume contraction, and this signals the kidneys to avidly retain sodium. This concomitant retention of water and sodium is appropriate in this setting and is supported by a low urine sodium concentration (< 20 mmol/L) and, often, a low urine volume. Often the person who has a contracted ECF volume will drink water or another low-solute fluid (e.g., tea), which contributes further to the hyponatremia. These patients, by definition, have serum sodium and body water levels that are lower than normal but have more loss of sodium relative to loss of water.4,5

Normal or near-normal ECF volume

In the setting of hyponatremia and clinically normal or near-normal ECF volume, ADH release or renal tubular responsiveness to ADH may be unrelated to serum tonicity or ECF volume contraction. In these situations, the patient is said to have the syndrome of inappropriate secretion of ADH (SIADH) or “a reset osmostat”.3,6,7,8,9,10 In SIADH, the serum sodium concentration falls as the kidneys inappropriately retain free water. The patient’s normal amount of body sodium is functionally diluted by the retained water. The patient appears to have a normal ECF volume or mild ECF volume overload (“near normal”). The urine sodium concentration is typically greater than 40 mmol/L.

The many causes of SIADH () include almost any pulmonary or neurologic problem. Some lung cancers can produce ectopic ADH, which signals inappropriately to the kidney. Numerous medications can have an ADH-like effect on the renal tubules or potentiate the effect of endogenous ADH: some of the more common agents are presented in . Other stimuli include pain and excessive nausea and vomiting.11,12,13,14

Two other potential causes of hyponatremia in patients with normal or near-normal ECF volume are hypothyroidism and adrenal insufficiency. A diagnosis of SIADH can be made only when these conditions have been ruled out by appropriate tests (e.g., determining the serum concentration of thyroid stimulating hormone or performing the cortisol stimulation test) and cannot be made when the patient has renal failure or an abnormal ECF volume.

In the rarer setting of a reset osmostat, which can occur in various chronic and debilitating disease states, there is felt to be a lowered setting of osmoreceptors. In these cases, the receptors will stimulate ADH release at lower serum osmolalities. Typically this resetting is chronic and the diagnosis is suspected because the serum sodium concentration, although lower (typically 124–134 mmol/L), is stable and remains at these levels for long periods. By definition, as in the diagnosis of SIADH, these patients must have normal renal, thyroid and adrenal function. Although beyond the scope of this review, the diagnosis of reset osmostat can be made by challenging these patients with a water load and measuring the ability to maximally dilute the urine osmolality.3,4,5

Expanded ECF volume

The cause of this type of hyponatremia is usually easy to identify. Edema-producing states, such as chronic congestive heart failure, cirrhosis and nephrotic syndrome, can all cause hyponatremia. The patients have an ECF volume overload and an elevated body content of sodium and water but, by definition, have more water relative to sodium. However, these patients often have a low effective circulating volume and poor renal perfusion. Because the kidney does not distinguish between a low effective circulating volume and ECF volume contraction, it will avidly retain sodium and water, which leads to edema. The urine sodium concentration is usually less than 20 mmol/L but may be higher if the patient is receiving diuretic therapy. These patients may also have ECF volume contraction from correctible causes and may respond to a gentle oral challenge of isotonic salt and water. Nephrotic syndrome can be ruled out by testing a urine sample and a 24-hour urine collection for protein; the 24-hour amount will be greater than 3.0 g in nephrotic syndrome.

Rarely, in the outpatient setting, a patient will present with hyponatremia secondary to psychogenic polydipsia. Typically seen in patients with schizophrenia or other psychiatric diseases, this disorder is due to ingestion of large volumes of water (> 20 L) over a short period. The hyponatremia, which can cause confusion or seizures, develops temporarily and resolves quickly as the kidneys work to excrete the excessive free water.4,5,7 The urine is dilute (osmolality < 100 mOsm/L), as is the serum (normal range, 280–295 mOsm/L).

Management

The key to effective management of hyponatremia is establishing the type and its cause, so that the cause can be removed, if possible, and the management will be appropriate. Paramount is clarifying whether the hyponatremia has developed quickly (over a few days) and is acute or whether it has developed over days to weeks and is chronic. The rapidity of correction of the serum sodium concentration should be closely linked to the suspected time over which the hyponatremia has developed.

If the patient has only mild symptoms of hyponatremia (headache, lethargy, dizziness), or is asymptomatic, and the hyponatremia is not severe (sodium level > 125 mmol/L), we recommend a conservative approach. Discontinuation of all possible offending drugs is important. In SIADH or the edema-producing states, a trial of water restriction to less than 1 to 1.25 L/d (depending on the degree of hyponatremia) can be attempted; the serum sodium level should be measured at regular intervals to look for improvement.4,8,9,10,11,12

If the serum sodium level continues to fall, the patient may require an intravenous trial of normal saline to clarify the diagnosis. If the patient has ECF volume contraction (which may not be clinically apparent), a trial of saline will always improve the serum sodium level. If the patient has SIADH, the hyponatremia will worsen. The trial should be done with caution, following the “rules” for sodium correction (). Rapid correction can result in osmotic demyelination syndrome, with resultant severe brain injury and potentially death.9,10,11,12,15

Hyponatremia that has developed slowly (over several weeks) must be clearly distinguished from acute, newly developed hyponatremia. Patients with chronically low serum sodium concentrations tend to be the least symptomatic and are at highest risk of severe side effects if the sodium concentration is corrected too rapidly.16,17,18,19,20,21,22,23,24

The long-term management of SIADH can be difficult when no offending agent can be found or the process at work is not reversible (as with bronchogenic or other carcinomas). It is possible to inhibit the renal effects of ADH with lithium carbonate, but this agent has a narrow therapeutic index.19 Demeclocycline (a tetracycline), 600 mg daily, may also be used, since it inhibits cyclic adenosine monophosphate, which diminishes the intracellular effects of ADH on the renal tubular cells.19

The management of hyponatremia in patients with hypervolemia can be difficult. Water restriction to less than 1.25 L/d is essential. Sodium restriction to 70 mmol/d (with the aid of a dietitian) will help with edema. A loop diuretic should be used to promote sodium and water excretion by the kidneys. In both congestive heart failure and cirrhosis, the addition of a potassium-sparing diuretic is useful to prevent hypokalemia and lessen edema (and ascites). Referral to a cardiologist or hepatologist may be necessary in cases of refractory heart failure or cirrhotic ascites. Patients with nephrotic syndrome should be referred to a nephrologist, as specific therapies (e.g., with corticosteroids and immunosuppressive drugs) may be directed at the cause of their disease and reduce proteinuria.

presents a suggested management algorithm.

Fig. 1: Algorithm for the recommended management of hyponatremia. [Na+] = serum sodium concentration; ECF = extracellular fluid.

The case revisited

The patient has clinical signs of ECF volume contraction. The most likely cause is gastrointestinal losses of salt and water, with only water replacement. It is also likely that the thiazide diuretic is contributing to the hyponatremia. Thiazides impair the kidney’s ability to produce a dilute urine.19 Both thiazides and loop diuretics (e.g., furosemide) impair the kidney’s ability to reabsorb sodium, but thiazides also impair free water excretion.24,25 With continued fluid intake and impaired excretion of water, hyponatremia can develop rapidly. The ECF volume contraction, diarrheal losses and diuretic use have also resulted in hypokalemia in this patient. As ECF volume contraction develops, the kidneys actively excrete potassium in exchange for sodium in an attempt to preserve ECF volume.

Another factor potentially contributing to this patient’s hyponatremia may be the “tea and toast” phenomenon. In elderly patients with a diet poor in protein and sodium, hyponatremia may be worsened by their low solute intake. The kidney’s need to excrete solutes aids in water excretion. An increase in dietary protein and salt can help improve water excretion. By a mechanism similar to that in the “tea and toast” phenomenon, hyponatremia can occur with excessive beer drinking, although this was unlikely in our patient. “Beer-drinker’s potomania” is caused by a beer “diet” that is high in fluid but low in solute. In both situations, a 24-hour urine collection will reveal a solute excretion of less than 500 mOsm/d.

The management of our patient should include temporary discontinuation of the thiazide diuretic. Although her hyponatremia has developed over about a week, she has clear evidence of ECF volume contraction. Volume restoration with normal saline and potassium replacement is required until the postural drop in blood pressure is less than 10 mm Hg. She should then be treated conservatively with oral sodium and potassium replacement. She should be reassessed frequently to ensure improvement. An alternative medication should be sought to treat her systolic hypertension. 26 If the thiazide diuretic is to be reintroduced, measurement of the serum electrolyte concentrations should be undertaken 5–7 days later to ensure that hyponatremia has not recurred.

Footnotes

This article has been peer reviewed.

Contributors: Dr. Yeates was the principal author and revised and prepared the final version. Dr. Morton assisted in redesigning the algorithms and boxes. Drs. Morton and Singer critically reviewed and revised the article for important intellectual content. All authors approved the version to be published.

Competing interests: None declared.

Correspondence to: Dr. Karen E. Yeates, University Health Network, 620 University Ave., Toronto, ON M5G 2C1

References

1. Haralampos J, Milionis GL, Elisaf MS. The hyponatremic patient: a systematic approach to laboratory diagnosis [review]. CMAJ 2002;166(8):1056-62. [PMC free article] [PubMed]2. Palmer BF. Hyponatremia in neurosurgical patients: syndrome of inappropriate antidiuretic hormone versus cerebral salt wasting. Nephrol Dial Transplant 2000;15:262-8. [PubMed]3. Kahn T. Reset osmostat and salt and water retention in the course of severe hyponatremia. Medicine (Baltimore) 2003;82:170-6. [PubMed]

4. Halperin M, Goldstein M. Fluid, electrolyte and acid-base physiology: a problem based approach. 3rd ed. Philadelphia: WB Saunders Company; 1998.

5. Preston R. Acid-base, fluids and electrolytes made ridiculously simple. Miami: Medmaster; 1997.

6. Adrogue HJ, Madias NE, Hyponatremia. N Engl J Med 2000;342:1581-86. [PubMed]7. Chung HM, Kluge R, Schrier R. Clinical assessment of extracellular fluid volume in hyponatremia. Am J Med 1987;83:905-8. [PubMed]8. Anderson RJ. Hospital associated hyponatremia. Kidney Int 1986;29:1237-47. [PubMed]9. Sterns RH, Cappuccio JD, Silver SM, Cohen EP. Neurologic sequelae after treatment of severe hyponatremia: A multicenter perspective. J Am Soc Nephrol 1994;4:1522-30. [PubMed]10. Sterns RH, Thomas DJ, Herndon RM. Brain dehydration and neurologic deterioration after correction of hyponatremia. Kidney Int 1989;35:69-75. [PubMed]11. Berl T. Treating hyponatremia: Damned if we do and damned if we don’t [review]. Kidney Int 1990;37:1006-18. [PubMed]12. Laureno R, Karp BI. Myelinolysis after correction of hyponatremia. Ann Intern Med 1997;126:57-62. [PubMed]13. Holden R, Jackson MA. Near-fatal hyponatremic coma due to vasopressin over-secretion after “ecstasy” (3,4-MDMA). Lancet 1996;347:1052-3. [PubMed]14. Maesaka JK. An expanded view of SIADH, hyponatremia and hypouricemia. Clin Nephrol 1996;46:79-83. [PubMed]15. Ayus JC, Arieff AI. Chronic hyponatremic encephalopathy in postmenopausal women: association of therapies with morbidity and mortality. JAMA 1999; 281:2299-304. [PubMed]16. Strange K. Regulation of solute and water balance and cell volume in the central nervous system. J Am Soc Nephrol 1992;3:12-27. [PubMed]17. Ellis SJ. Severe hyponatremia: complications and treatment. Q J Med 1995; 88:905-9. [PubMed]18. Ayus JC, Wheeler JM, Arief AI. Postoperative hyponatremia encephalopathy in menstruant women. Ann Intern Med 1992;117:891-7. [PubMed]19. Forrest JN, Cox M, Hong C, et al. Superiority of demeclocycline over lithium in the treatment of chronic syndrome of inappropriate secretion of antidiuretic hormone. N Engl J Med 1978;298:173-81. [PubMed]20. Arieff AI. Hyponatremia, convulsions, respiratory arrest, and permanent brain damage after elective surgery in healthy women. N Engl J Med 1986;314: 1529-40. [PubMed]21. Sterns RH. The management of symptomatic hyponatremia. Semin Nephrol 1990;10:503-14. [PubMed]22. Sterns RH. The treatment of hyponatremia: First do no harm. Am J Med 1990;88:557-60. [PubMed]23. Lien YH, Shapiro JI, Chan L. Study of brain electrolytes and osmolytes during correction of chronic hyponatremia. Implications for the pathogenesis of central pontine myelinolysis. J Clin Invest 1991;88:303-9. [PMC free article] [PubMed]24. Friedman E, Shadel M, Hallan H, Fardel Z. Thiazide induced hyponatremia. Reproducibility by single-dose challenge and analysis of pathogenesis. Ann Intern Med 1989;110:24-9. [PubMed]25. Clark BA, Shannon RP, Rosa RM, Epstein FH. Increased susceptibility to thiazide induced hyponatremia in the elderly. J Am Soc Nephrol 1994;5: 1106-11. [PubMed]26. Campbell NRC, Drouin D, Feldman RD; Canadian Hypertension Recommendations Working Group. The 2001 Canadian hypertension recommendations: take-home messages [erratum in CMAJ 2002;167(9):989]. CMAJ 2002;167(6):661-8. [PMC free article] [PubMed]

Diagnosis and Management of Sodium Disorders: Hyponatremia and Hypernatremia

1. Hoorn EJ,

et al.
Hyponatremia and mortality: moving beyond associations. Am J Kidney Dis.
2013;62(1):139–149….

2. Mannesse CK,

et al.
Prevalence of hyponatremia on geriatric wards compared to other settings over four decades: a systematic review. Ageing Res Rev.
2013;12(1):165–173.

3. Gankam-Kengne F,

et al.
Mild hyponatremia is associated with an increased risk of death in an ambulatory setting. Kidney Int.
2013;83(4):700–706.

4. Hawkins RC.
Age and gender as risk factors for hyponatremia and hypernatremia. Clin Chim Acta.
2003;337(1–2):169–172.

5. Crestanello JA,

et al.
Preoperative hyponatremia predicts outcomes after cardiac surgery. J Surg Res.
2013;181(1):60–66.

6. Crestanello JA,

et al.
Does preoperative hyponatremia potentiate the effects of left ventricular dysfunction on mortality after cardiac surgery? J Thorac Cardiovasc Surg.
2013;145(6):1589–1594, 1594e1–1594e2.

7. Vaishya R,

et al.
Mortality predictions in severe hyponatraemia in emergency inpatients. J Indian Med Assoc.
2012;110(2):94–97.

8. Shchekochikhin DY,

et al.
Outcome differences in community- versus hospital-acquired hyponatremia in patients with a diagnosis of heart failure. Circ Heart Fail.
2013;6(3):379–386.

9. Hagino T,

et al.
Hyponatremia at admission is associated with in-hospital death in patients with hip fracture. Arch Orthop Trauma Surg.
2013;133(4):507–511.

10. Korkmaz I,

et al.
Baseline characteristics and the association between hyponatraemia and pulmonary embolism prognosis. J Pak Med Assoc.
2013;63(3):331–335.

11. Assadi F.
Hyponatremia: a problem-solving approach to clinical cases. J Nephrol.
2012;25(4):473–480.

12. Pfennig CL,

et al.
Sodium disorders in the emergency department: a review of hyponatremia and hypernatremia. Emerg Med Pract.
2012;14(10):1–26.

13. Verbalis JG,

et al.
Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med.
2013;126(10 suppl 1):S1–S42.

14. Spasovski G,

et al.;
Hyponatraemia Guideline Development Group.
Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol.
2014;170(3):G1–G47.

15. Masri G, et al. Evaluation of hyponatremia. https://online.epocrates.com/noFrame/showPage?method=diseases&MonographId=57 [subscription required]. Accessed October 8, 2014.

16. Sarikonda KV, et al. Hyponatremia. http://www.essentialevidenceplus.com/content/eee/146 [subscription required]. Accessed October 8, 2014.

17. Imbriano LJ,

et al.
Normal fractional urate excretion identifies hyponatremic patients with reset osmostat. J Nephrol.
2012;25(5):833–838.

18. Carvounis CP,

et al.
Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure. Kidney Int.
2002;62(6):2223–2229.

19. Albert NM,

et al.
A randomized controlled pilot study of outcomes of strict allowance of fluid therapy in hyponatremic heart failure (SALT-HF). J Card Fail.
2013;19(1):1–9.

20. Sterns RH,

et al.
The treatment of hyponatremia. Semin Nephrol.
2009;29(3):282–299.

21. Sood L,

et al.
Hypertonic saline and desmopressin: a simple strategy for safe correction of severe hyponatremia. Am J Kidney Dis.
2013;61(4):571–578.

22. Hew-Butler T,

et al.
Consensus statement of the 1st International Exercise-Associated Hyponatremia Consensus Development Conference, Cape Town, South Africa 2005. Clin J Sport Med.
2005;15(4):208–213.

23. Moritz ML,

et al.
100 cc 3% sodium chloride bolus: a novel treatment for hyponatremic encephalopathy. Metab Brain Dis.
2010;25(1):91–96.

24. Cárdenas A,

et al.
Tolvaptan, an oral vasopressin antagonist, in the treatment of hyponatremia in cirrhosis. J Hepatol.
2012;56(3):571–578.

25. Hauptman PJ,

et al.;
EVEREST Investigators.
Clinical course of patients with hyponatremia and decompensated systolic heart failure and the effect of vasopressin receptor antagonism with tolvaptan. J Card Fail.
2013;19(6):390–397.

26. Schrier RW,

et al.;
SALT Investigators.
Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. N Engl J Med.
2006; 355(20):2099–2112.

27. Josiassen RC,

et al.
Vaptans: a potential new approach for treating chronic hyponatremia in psychotic patients. Clin Schizophr Relat Psychoses.
2012;6(1):21–26.

28. Berl T;
SALTWATER Investigators.
Oral tolvaptan is safe and effective in chronic hyponatremia [published correction appears in J Am Soc Nephrol. 2010;21(8):1407]. J Am Soc Nephrol.
2010;21(4):705–712.

29. Dahl E,

et al.
Meta-analysis: the safety and efficacy of vaptans (tolvaptan, satavaptan and lixivaptan) in cirrhosis with ascites or hyponatraemia. Aliment Pharmacol Ther.
2012;36(7):619–626.

30. Lehrich RW,

et al.
Role of vaptans in the management of hyponatremia. Am J Kidney Dis.
2013;62(2):364–376.

31. Mc Causland FR,

et al.
Association of serum sodium with morbidity and mortality in hospitalized patients undergoing major orthopedic surgery. J Hosp Med.
2014;9(5):297–302.

32. Leung AA,

et al.
Preoperative hypernatremia predicts increased perioperative morbidity and mortality. Am J Med.
2013;126(10):877–886.

33. Adrogué HJ,

et al.
Hypernatremia. N Engl J Med.
2000;342(20):1493–1499.

34. Funder JW,

et al.
Case detection, diagnosis, and treatment of patients with primary aldosteronism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab.
2008;93(9):3266–3281.

35. Sands JM,

et al.;
American College of Physicians; American Physiological Society.
Nephrogenic diabetes insipidus. Ann Intern Med.
2006;144(3):186–194.

36. Reynolds RM,

et al.
Disorders of sodium balance. BMJ.
2006;332(7543):702–705.

37. Kahn A,

et al.
Controlled fall in natremia and risk of seizures in hypertonic dehydration. Intensive Care Med.
1979;5(1):27–31.

What is hyponatremia and how can you avoid it? by Precision Hydration

Hyponatremia hit the headlines with the publication of data on the prevalence of the condition in Ironman finishers. Scarily, over 10% of athletes tested had hyponatremia!

But what is this potentially race-ruining condition and how can it be avoided?

Contents:

What is hyponatremia?

Hyponatremia is a medical term describing low (hypo) blood sodium levels (natremia – Na is the chemical symbol for sodium).

There are a few different causes of the condition, but the one of interest to athletes is when dilution of sodium levels in the blood is driven by excessive drinking. This can be exacerbated by the loss of sodium in sweat during prolonged exercise. This variant of the condition is known as ‘Exercise Associated Hyponatremia’, or EAH.

The symptoms of hyponatremia

Maintaining blood sodium levels within a healthy range (135-145mmols per litre) is critical to homeostasis and optimal bodily function. When blood sodium levels drop below this ideal range initial symptoms can include:

  • Nausea
  • Lethargy
  • Muscle cramps
  • Weakness/fatigue
  • Headaches
  • Restlessness

Because of how finely balanced your blood sodium levels need to be for good health, even mild hyponatremia during exercise is bad news. It can seriously undermine your performance well before it starts to make you properly ill.

In severe cases of hyponatremia, the symptoms can potentially escalate into seizures and coma. The end result can even be death, if things go uncorrected for long enough. This is because, in order to try to preserve sodium concentrations in the blood, the body shifts excess fluid it can’t otherwise excrete from the blood plasma into it’s own cells, causing them to swell up.

This swelling is devastating when it occurs in brain cells and is what leads to the condition becoming fatal. About 14 deaths, including one at Ironman Frankfurt in 2015, have been directly attributed to hyponatremia during sporting events since 1981. However, as the results from the recent Ironman study show, the occurrence of non-fatal EAH is likely to be a lot higher.

What causes hyponatremia?

As already alluded to, for athletes the primary cause of hyponatremia is the over-consumption of fluids (especially drinks low in sodium).

A popular theory has emerged that the prevalence of over-drinking (and therefore hyponatremia) has increased in recent decades because the pitfalls of dehydration have been so effectively publicised since the 1980s that most athletes believe that they need to drink well before they feel thirsty, and that a ‘more is better’ approach applies to hydration.

In my conversations with athletes I do see many of them drinking very large amounts routinely in an attempt to make sure their pee is ‘clear’ all of the time, as they see this as a primary indicator of being ‘well hydrated’. And that applies right up to the pro level.

So, I would say that there’s still widespread lack of appreciation of the fact that too much fluid intake can be as detrimental for health and performance as too little. But this is slowly starting to change with more publicity about hyponatremia in the non-scientific press as sports like triathlon have become more popular.

Many experts also feel that the very large sodium losses in sweat seen in some individuals – as a result of high sweat rates over long periods of time and/or the very high sweat sodium concentrations – can contribute to increased susceptibility to developing hyponatremia. And I agree with that.

There are quite a lot of interesting case studies that back this up, both in healthy people with high sweat/sodium losses and those with Cystic Fibrosis, who’s genetic disorder causes them to lose lots of sodium in their sweat.

However, it’s also fair to say that this area is the subject of ongoing debate.

How can you avoid hyponatremia?

In theory, avoiding hyponatremia is pretty straightforward, you just have to avoid drinking more than you sweat and pee out, so that dilution of your blood does not occur.

For quite a while some experts (notably Prof Tim Noakes, with many others following his lead) have been advocating a ‘drink water to thirst’ approach for this very reason. When healthy people drink water purely to the dictates of thirst during exercise, it has been demonstrated time and again that they don’t tend to take in more than they sweat out and, as a result, become gradually dehydrated, making hyponatremia all but impossible.

This strategy is often backed up with evidence to support the fact that that mild dehydration does not necessarily negatively impact performance. That’s almost certainly true to a degree and if you’re keen to dive deeper into that topic you can read my thoughts here

But this approach leaves athletes to train for and compete in any event, of any length or intensity, and in all conditions, with nothing more than this relatively vague statement to guide their hydration strategy.

It also ignores the valuable contribution of supplementing fluid intake with additional sodium to help aid fluid retention, maintain blood sodium levels and replace some of that lost in sweat. At a certain point the usefulness of ‘drink to thirst’ guidelines effectively ends. And that point is probably when you’re exercising for more than 2 hours, assuming you began well hydrated (for advice on how to do that, this blog is worth a read).

Should I just drink to thirst to avoid hyponatremia?

If avoiding hyponatremia is your one and only objective, then drinking to thirst is probably ok advice to follow. But, in my view, it starts to get more complicated when you consider that most athletes want to perform at their best, not just ‘survive’ a race.

Yes, dehydration has historically been over emphasised, but it can, beyond a certain point, still cause massive performance issues primarily because it manifests itself in reduced blood volume and increased blood viscosity (thickness), both of which impair cardiovascular function and heat dissipation. Anyone who has become dehydrated and tried to exercise effectively will know this only too well!

The negative effects of dehydration are especially relevant in events that are very long and hot (such as Ironman races and ultra marathons) and for athletes who’re training hard and sweating a lot on back to back days. That’s because, in these scenarios, the volume of sweat and sodium losses can be quite dramatic.

Simply drinking water ‘to thirst’ on these occasions is not always adequate to maintain blood plasma volumes to a degree that’s compatible with peak performance. It’s a lot more productive to think of dehydration as existing on the opposite end of the scale to hyponatremia, and to aim to strike a balance between these two extremes.

The role of sodium in avoiding hyponatremia

It’s long been known that taking sodium in with drinks increases fluid retention in the blood stream. Also, sweat contains a relatively large (and variable) amount of sodium in it so, when sweat output is high, the net loss of sodium can be substantial too.

Sodium is a finite resource in the body and, as a result, supplementation can help to maintain both blood volume and blood sodium levels much better than drinking water alone, especially at times when sweat losses are high.

Sodium also helps reduce the rate of dilution in the bloodstream when compared to just taking in water alone. This was shown very neatly in a 2015 study where triathletes were given either extra sodium supplements or a placebo pill to take alongside regular sports drinks during a middle distance race in hot weather.

The ‘extra sodium’ group replaced around 71% of their sodium losses during the event, with the ‘placebo’ group only replacing about 20%. The results showed better maintenance of blood volume, higher blood sodium levels post-race and faster finishing times in the sodium group than in those taking the placebo.

Personalizing your sodium intake

Where I would go one step further with this argument is in the idea of personalising your sodium supplementation to take into account your personal fluid and sodium losses.

The amount of sodium you lose in your sweat can vary massively from athlete to athlete and sweat rates can also vary dramatically. We’ve tested athletes who lose an estimated 40 grams of sodium in the course of a single ten hour Ironman, compared with others who lose just 3 grams during the same period.

The idea that a single strategy for fluids and sodium supplementation could work equally well for both of these athletes makes no sense at all. You can start to understand your individual electrolyte needs by taking our free online Sweat Test or you can find out exactly how much sodium you lose in your sweat by taking our Advanced Sweat Test.

Whilst sodium supplementation should not be seen as a way to compensate for over-drinking to avoid hyponatremia, it can be extremely useful in helping to maintain hydration levels at times when your sweat losses are high. It helps by increasing the retention of fluid in your bloodstream and maintaining your blood sodium levels.

So, personalising your sodium and fluid intake not only reduces the risk of hyponatremia, but maximise your performance when sweat losses are high. Personalisation is best achieved through a combination of data collection (taking a Sweat Test) and some good ol’ fashioned trial and error in training and events.

Further Reading

Hyponatremia – Endocrine and Metabolic Disorders

Hypertonic (3%) saline (containing 513 mEq sodium/L [513 mmol/L]) use requires frequent (every 2 hours) electrolyte determinations. In some situations, hypertonic saline may be used with a loop diuretic. Equations are available to help predict the sodium response to a given amount of hypertonic saline, but these formulas are only rough guidelines and do not decrease the need to monitor electrolyte levels frequently. For instance, in hypovolemic hyponatremia the sodium level can normalize too quickly as volume is replaced and thus removes the hypovolemic stimulus for vasopressin secretion, causing the kidneys to excrete large amounts of water.

Another recommendation includes administration of desmopressin 1 to 2 mcg every 8 hours concurrently with hypertonic saline. The desmopressin prevents an unpredictable water diuresis that can follow the abrupt normalization of endogenous vasopressin that can occur as the underlying disorder causing hyponatremia is corrected. After the sodium has been corrected at the appropriate rate for 24 hours, desmopressin is stopped. Hypertonic saline can then be stopped, or, if required for continuing correction of hyponatremia, continued..

For patients with rapid-onset hyponatremia and neurologic symptoms, rapid correction is accomplished by giving 100 mL of hypertonic saline IV over 15 minutes. This dose can be repeated once if neurologic symptoms are still present.

For patients with seizures or coma but slower onset hyponatremia, ≤ 100 mL/hour of hypertonic saline may be administered over 4 to 6 hours in amounts sufficient to raise the serum sodium 4 to 6 mEq/L (4 to 6 mmol/L). This amount (in mEq OR mmol) may be calculated using the sodium deficit formula as

where TBW is 0.6 × body weight in kg in men and 0.5 × body weight in kg in women.

For example, the amount of sodium needed to raise the sodium level from 106 to 112 mEq/L in a 70-kg man can be calculated as follows:

Because there is 513 mEq (mmol) sodium/L in hypertonic saline, roughly 0.5 L of hypertonic saline is needed to raise the sodium level from 106 to 112 mEq/L (mmol/L). To result in a correction rate of 1 mEq/L/hour, this 0.5 L volume would be infused over about 6 hours.

Patients meeting the criteria for cerebral salt wasting should not be fluid restricted because fluid restriction can cause brain vessel vasospasm. Although isotonic saline should correct the cause of hyponatremia, use of hypertonic saline is recommended to prevent more severe hyponatremia if indeed SIADH is present.

Hyponatremia – an overview | ScienceDirect Topics

1

Hyponatremia is defined as a serum sodium concentration below 135 mmol/L.

2

Hyponatremia is the most common electrolyte abnormality in hospitalized patients.

3

Patients with pseudohyponatremia have a normal serum sodium concentration, but the measured sodium level is falsely low. This artifact occurs when flame emission spectrometry is used to measure the serum sodium concentration in patients with severe hypertriglyceridemia or hyperparaproteinemia. Currently, most labs measure serum sodium with a sodium‐selective electrode method, which does not cause this artifact.

4

Evaluation of hyponatremia involves assessment of volume status.

5

In hypovolemic hyponatremia the urine sodium concentration is usually <20 mmol/L, but may be higher in some settings, such as with diuretic use.

6

Euvolemic hyponatremia can occur in patients with hypothyroidism, adrenal insufficiency, a reset osmostat, and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

7

Causes of SIADH include medications, tumors, and pulmonary or neurological disease. In SIADH, the urine is inappropriately concentrated and the spot urine sodium concentration is usually >30 mEq/L. A diagnosis of SIADH requires exclusion of thyroid, adrenal, and renal dysfunction.

8

Hypervolemic hyponatremia can occur in patients with heart failure, cirrhosis, and the nephrotic syndrome. The urine sodium concentration is usually <20 mmol/L.

9

Hyperglycemia causes dilutional hyponatremia. The serum sodium is lowered by 1.6 mmol/L for every 100 mg/dL increase in blood glucose over 100 mg/dL.

10

Most patients with mild hyponatremia are asymptomatic. Symptoms of rapid‐onset and more severe hyponatremia include nausea, vomiting, lethargy, headache, restlessness, disorientation, and muscle cramps.

11

Initial laboratory testing for patients with hyponatremia should include electrolytes with glucose, serum osmolality, spot urinary sodium concentration, and assessment of thyroid and adrenal function (if applicable). Spot urine osmolality is only sometimes helpful because almost all cases of hyponatremia are associated with inappropriately concentrated urine.

12

Cerebral edema can occur when acute (<48 hours) hyponatremia is not treated promptly and may cause increased intracranial pressure, seizures, coma, tentorial herniation, and death.

13

There is no consensus about the optimal treatment of acute, symptomatic hyponatremia. One proposed management plan is to initially raise the serum sodium by 2 mmol/L per hour using hypertonic (3%) saline.

14

Depending on the clinical circumstances, treatment options for patients with chronic (>48 hours) hyponatremia include fluid restriction, intravenous saline, oral salt tablets, and medications, such as demeclocycline and loop diuretics.

15

Fluid restriction is usually the most appropriate treatment for SIADH in addition to therapy directed at the underlying cause. Administration of normal saline can worsen the hyponatremia of SIADH.

16

With chronic hyponatremia, the sodium should be raised by, at most, 0.5 mmol/L/hr unless there are severe symptoms. In all cases of chronic hyponatremia, the sodium should be raised by no more than 12 mmol/L/day.

17

Neuronal demyelination (myelinolysis) is a devastating neurologic complication that can occur when chronic hyponatremia is corrected too quickly.

Dehydration and Hyponatremia: How Common? How Dangerous?

Yesterday Gretchen Reynolds and I blogged more or less simultaneously about fluid consumption issues while running, particularly while marathoning. Gretchen’s blog appeared here on the New York Times website; and mine here at RunnersWorld.com.
Gretchen wrote primarily about studies showing that some people drink too much in marathons, and become hyponatremic (too much water in blood, too little salt). But she also mentioned that some runners don’t understand the importance of hydration, and perhaps don’t drink enough.
I wrote a more technical piece illustrating hydration strategies that would result in a two- to three-percent weight loss during a marathon. This is now accepted as a generally safe level of dehydration in a marathon. (Note: Not all body-weight loss in a marathon is water loss. Some is tissue loss.)
Now would be a good time to step back and ask the more general questions. What percent of marathoners get hyponatremic? What percent get dehydrated? What are the effects of each?
Hyponatremia is a classified medical diagnosis that has been fairly extensively studied in endurance events in the last decade. Results have shown anywhere from .1 percent of endurance athletes to 50 percent (in a 100-miler) are hyponatremic at the finish. The most famous study, involving the 2002 Boston Marathon, found an incidence of 13 percent. Many runners, including me, were stunned by the reports of gross overdrinking.
However, it’s important to note that you can be hyponatremic without being sick or in danger, and this is in fact the case for the vast majority of cases mentioned above. Having modest hyponatremia (sodium <135 mE/L) is like having modestly high blood pressure. It’s not good, but you’re still alive and probably don’t even know you have it.
Very severe hyponatremia (<130 mE/L; or, far worse, <125 mE/L) can be life threatening. Indeed, there have been eight recorded deaths from hyponatremia in endurance athletes in the last several decades. Most of these severe cases are caused by extremely high fluid-drinking rates during the event. (However, there are other genetic-type causes as well, and it’s even possible to be hyponatremic and dehydrated at the same time.)
Given the low to modest percentage of hyponatremia cases in marathons, it’s obvious that the vast majority of us finish at the same weight we started or (probably) somewhat dehydrated. But dehydration doesn’t exist as a medical condition. It’s not dangerous in the short-term (a day or two). It’s completely normal for humans to get dehydrated during the day as we rush around taking care of our various responsibilities. Then at night, when we relax, we notice that we’re thirsty and start drinking. End of dehydration.
Of course, a marathon exists in a compressed time period, of say two to five hours, and our heavy sweating rate makes it possible to get dehydrated quite quickly. Then what happens? Basically nothing. We simply slow down a little as our blood grows thicker and the heart has to pump harder to push it around. What about death by heatstroke? Some would argue this, but the direct link appears to be quite weak. Heatstroke can be deadly in rare cases, but it’s not at all clear that it’s caused by dehydration.
How about muscle cramps? Again, the link to dehydration is weak. How about bonking? Nope. The link is much more likely to be low carbs than dehydration.
Now, I can virtually guarantee that if you run a marathon, you will reach a point where your body just doesn’t want to go any farther. I can also virtually guarantee that the cause is not dehydration. It’s much more likely to be low carbs and/or muscle fatigue, neither of which will be helped by drinking water.
In summary, what I’m trying to say here is that just about everyone has some degree of hyponatremia or dehydration at the end of a marathon. And 99 percent of the time, nothing happens. Of the two, hyponatremia is the more serious. If your stomach is sloshing ominously and the rings on your fingers are getting tight, stop running and seek medical attention.
A final note: There are three primary causes of death during a marathon. All begin with an “H.” They are, in order of incidence, heart attack, hyponatremia, heatstroke. You can’t really prevent a heart attack or heatstroke; they happen too quickly. You can usually prevent hyponatremia by being careful not to drink too much. So be careful.

This content is created and maintained by a third party, and imported onto this page to help users provide their email addresses. You may be able to find more information about this and similar content at piano.io

Hyponatremia | Jeff Galloway

Hyponatremia or Water Intoxification- Are You Drinking Too Much Water?

While extremely rare, this condition has caused death during or after running long runs or marathons. Many runners become overly concerned about hyponatremia, and don’t drink enough before during and after a long run. The result is dehydration, which is much more likely to cause medical problems, and increase recovery time after long runs. As in all training components, each runner must assume responsibility for their hydration and health, and use good common sense.

The underlying cause of hyponatremia is often severe dehydration, compounded by consuming only water in great quantities. Every marathoner should be aware of this condition, not only for self-protection. If you see someone who seems to be going through the symptoms, a little attention can bring them around relatively quickly. If a member of your running group shows any of the below symptoms, stay in touch with them for the next few hours to ensure that they are getting what they need and are not alone. As always, when in doubt, get medical advice and care. A physician will have to determine whether an IV will help or not.

Causes:

  • Starting the run, already dehydrated, due to consuming alcohol the night before, not drinking enough fluid the day before, or eating a very salty meal the night before.
  • Sweating excessively and continuously for more than 5 hours.
  • Taking medication which messes up the fluid storage, and fluid balance systems, within 48 hours of a long run when
  • Drinking too much water, in a period of 1-2 hours, once the body is dehydrated

Signs that you may have it:

  • hands and/or feet swell up twice normal size (or more)
  • nausea that leads to vomiting, continuous or several times
  • diarrhea which is continuous or repeated every 10 min or so
  • Mental disorientation and confusion
  • Severe cramping of the muscles for several miles
  • Disorientation with any of the above symptoms

How to avoid it:

1. The day before, drink a hydration drink, such as Accelerade, 6-8 oz an hour, unless you hear “sloshing” in your stomach

2. Drink water in small doses during a long run—4-6 oz, no more often than every 20 minutes (12 min on a hot day)

3. Don’t drink if you hear a sloshing sound in your stomach

4. After 2-3 hours of continuous, excessive sweating, eat salty pretzels, or Mix a small packet of salt with your water, every 30 min or so

5. Continue to eat or drink the salty food for an hour after a 5 hour plus long run

6. Drink several sips of water or electrolyte drink (Accelerade recommended) with every pretzel, or put ½ tsp of table salt in a glass of water.

7. At the end of long runs, and for hours afterward, even if you are very thirsty, don’t drink more than 8 oz of water about every 20 min. It is better to drink some electrolyte beverage like Accelerade.

8. The electrolyte beverages don’t have enough sodium to get you back to balance, but the carbohydrate in them will slow down the absorption of the water.

9. Keep eating salty foods for an hour or more after a 5 hour plus long run.

Specifics, from the American College of Sports Medicine as verified by Biochemist Dr. Bill Vaughn, PhD

1. Drink about 17 oz of fluid, prior to 2 hours before the start. This allows the fluid to get into the system, with time for the excess to be eliminated.

2. Drink early and regularly during the long run, consuming 20-40 oz of fluid per hour. This is a lot less than many of our runners are drinking. This works out to 4-7 oz per mile for most runners.

3. Some carbohydrate with the drink–as in the GU type products, will help the re-hydration process, but only a little is needed (in my experience, one-third to one fourth of a packet per mile of GU.

4. Sodium is definitely recommended: 500-700mg per hour, in the form of pretzels, salt in the water or buffered salt tablets. (Succeed)

* On hot days, have a “weigh in” at the beginning and at the 3-4 hour and after marks. Weight loss of 6% or more has been a good indicator of serious problems.

* No medication, within 48 hours of the start of the long run, unless with a doctor’s permission. There has been at least one death tied to ibuprophen.

* I continue to hear of problems when runners eat a big meal the night before. It’s always best to snack from about noon until bedtime–and avoid alcohol.

Page not found |

Page not found |



404. Page not found

Monthly archive

MonTueWedThuFtSaSun

22232425262728

2930

12

12

1

3031

12

15161718192021

25262728293031

123

45678910

12

17181920212223

31

2728293031

1

1234

567891011

12

891011121314

11121314151617

28293031

1234

12

12345

6789101112

567891011

12131415161718

19202122232425

3456789

17181920212223

24252627282930

12345

13141516171819

20212223242526

2728293031

15161718192021

22232425262728

2930

Archives

Tags

Settings
for visually impaired

90,000 HYPONATREMIA IN ATHLETES ENDURANCE

In one of the publications, we have already covered in some detail the effect of dehydration on the physical condition of an athlete and his performance, both during the training process and during the competition.

In this same publication, we will touch upon another, very important topic for all athletes, without exception, practicing endurance sports (marathon, ultramarathon, ultratrail, triathlon, etc.), namely the state hyponatremia .

Hyponatremia is one of the most common (more than 75% of all finishers) medical complications among any endurance sports, moreover, it ranks first among them in the number of fatalities.

HYPONATREMIA DEVELOPS IN ALL ATHLETES PRACTICEING ULTRA DISTANCES, BUT AS A RULE, IT PROCEEDS WITHOUT SYMPTOM.

In this material, we do not consider hyponatremia developing in patients with various kinds of pathologies, for example, heart or renal failure, liver diseases, and a number of other diseases. The hyponatremia that develops in a healthy athlete practicing disciplines requiring endurance will be considered.

A LITTLE OF THEORY.

Blood plasma is a complex solution containing positively (sodium, potassium, magnesium) and negatively charged particles (chlorine, sulfates, phosphates, etc.). In addition to electrolytes, blood plasma also contains non-electrolytes – for example, proteins, oxygen, carbon dioxide.

One of the most important properties of plasma is its OSMOLARITY – an indicator of water-electrolyte metabolism, which affects the movement of fluid in the human body. The osmotric pressure is created when the solution is separated from the pure solvent by a membrane that is freely passable for the solvent, but impermeable to solutes. In the human body, water acts as a solvent, which freely passes through the cell membranes in any direction, depending on the osmotic pressure.

Normally, the osmotic pressure of the intracellular and extracellular space is in dynamic equilibrium. If in one of the spaces the osmolarity rises, then the water will pass into this space from another space with a lower osmolarity. Roughly speaking, imagine a glass divided from top to bottom by a membrane that is freely permeable to liquid. On both sides of the membrane there is an aqueous solution with sugar molecules dissolved in it (they cannot pass through the membrane).If the content of sugar molecules on one side of the membrane becomes greater (that is, the solution is more concentrated there), then water will flow through the membrane into this part of the glass, and will flow until the concentration of the solution is equalized on both sides of the membrane. This is osmolarity.

Among the whole variety of plasma components, there are three substances that actively influence, and in fact determine the osmolarity of the plasma, and therefore the movement of water in the human body – these are SODIUM, UREA and GLUCOSE.

The osmolarity formula is as follows: 2x SODIUM + UREA + GLUCOSE.

The osmotic pressure of the plasma is maintained by the body within a fairly strict range (280-300 mmol / l), it is equal, as can be seen from the formula, to the sum of the concentration of osmotically active components. Since the content of sodium ions in plasma (135-140 mmol / l) exceeds the content of all other substances included in the osmolarity formula, its osmotic pressure depends on the sodium content in plasma.

Hyponatremia is a condition in which the concentration of sodium ions in the blood plasma falls below 135 mmol per liter, while the norm is 145-150 mmol per liter.It should be noted right away that this norm is relative, for example, in older people, symptoms of hyponatremia will develop already at 135 mmol / L, while in younger people, symptoms may not be detected, for example, up to 120 mmol / L.

At the same time, the vast majority of cases of hyponatremia in adults are associated with an increase in the activity of antidiuretic hormone (ADH). ADH is a hypothalamic hormone that regulates the balance of water in the body, but not salt. ADH increases the reabsorption (reabsorption of fluid from the anatomical structures of the body) of water by the kidneys (the kidneys begin to retain water).This process is activated with a significant loss of fluid volume by the body and a simple and effective treatment is the restoration of blood volume (not replenishment with water, namely with an electrolyte balanced solution!), Which thus serves to turn off the signal of ADH excretion.

Hyponatremia can be caused by two opposite physiological conditions – both an excess of fluid in the body, and its lack.

A LITTLE PRACTICE.

In 2002, during the Boston Marathon, the Massachusetts Medical Society conducted a multivariate study to identify risk factors associated with hyponatremia.A few days before the race, 766 amateur runners of different ages and genders completed the questionnaire procedure. At the finish of the marathon, 488 of them additionally passed a blood test. In 13% of cases, a state of hyponatremia was noted (plasma sodium content less than 135 mmol per liter), 0.6% had a critical state of hyponatremia (plasma sodium less than 120 mmol per liter).

The state of hyponatremia was associated with significant fluid intake during the race – more than 3 liters.In the vast majority of cases (95%), the state of hyponatremia was observed in slow female runners, with a finish time of 4 hours or more, with a low body mass index.

In 2003, 14 amateur runners with signs of hyponatremia were admitted to clinics in London after the end of the marathon. One young man subsequently died of complications.

After this incident, a study was conducted in which 88 volunteer runners took part, who, before the next marathon, underwent a medical examination, had blood tests, filled out questionnaires, etc.At the end of the trial, 11 runners, or 12.5%, had asymptomatic hyponatremia. On average, these runners consumed more fluids during the marathon and had more weight at the end of the race than before the start, although 4 out of 11 runners did not show any weight gain.

Finishers were surveyed in 2009 during the world famous Western States Endurance Run. The results showed that of the 47 participants in the study, 30% of the participants (14 people) had hyponatremia.The condition of hyponatremia was directly related to a loss of 3 to 6% of weight, and in most cases was observed in runners with less experience of finishing in 100 mile races. That is, in this case, in more experienced runners, we observe a state of hyponatremia, which develops against the background of dehydration.

The following study was conducted between 2000 and 2004 with participants in the Houston Marathon. Of the 96 runners who took part in the study, 22% (21 people) met the criteria for hyponatremia after the finish line.Again, hyponatremia was shown to be related to the time spent at a distance. Slow runners consume more fluids while running and are at higher risk of hyponatremia. It was noted that if a runner lost less than 0.75 kilograms of weight during a marathon, the risk of hyponatremia increased 7 times compared to runners who lost more than 0.75 kilograms of body weight.

Of the 26 cases of hyponatremia recorded at the 1998 San Diego Marathon, 23 were among women.Women experience hyponatremia much more often than men. With an increase in body weight of more than 4% during the test, the likelihood of developing a state of hyponatremia is 45%.

During the triathlon competition in New Zealand at the full “iron” distance (3.8 km. Swimming, 180 km. Bicycle, 42.2 km. Running), the data of 330 athletes out of 605 started were analyzed. Blood samples were taken to measure plasma sodium concentration. The data showed that plasma sodium concentration is inversely related to changes in body weight.Of the 330 finishers, 58 (18%) had hyponatremia, while only 18 or 31% sought medical help. Women are susceptible to hyponatremia three times more often than men, which is explained by a lower weight loss at a distance of -2.7% on average in women versus -4.3% in men. In 73% of cases, excess fluid intake was the cause of hyponatremia.

Another study conducted in 2000 at the Ironman Triathlon in South Africa showed a linear relationship between hyponatremia and weight loss.Athletes’ weighing and blood tests were carried out at registration and immediately after the finish. The work demonstrated that athletes’ body weight dropped significantly during the race and did not return to normal values ​​over the next 12 hours.

CONCLUSIONS.

As we noted above, the state of hyponatremia is a common condition for all athletes practicing sports for endurance, when they are at a distance of 4 hours or more. With an increase in the time spent at a distance, the likelihood of hyponatremia increases.

HYPONATREMIA CAUSED BY THE STATE OF HYPERHYDRATION (excessive fluid intake) is more common in untrained and slow runners (time on a marathon more than 4 hours), who consume a large amount of fluid disproportionate to losses during a long distance, which leads to an imbalance in fluid balance in the body. Women are three times more likely to have fluid-induced hyponatremia than men. The reasons for this are a lower body mass index and less muscle mass.The state of hyponatremia against the background of excessive fluid intake is the most dangerous, as it can cause cerebral edema and death.

HYPONATREMIA CAUSED BY A STATE OF HYPOHYDRATION OR DEHYDRATION OF THE BODY is most often found in trained runners practicing ultra-distance from 100 kilometers and above, as well as in Ironman triathletes. Intense physical effort for a long time and insufficient fluid intake leads to a loss of body weight from 3 to 6 percent, triggering the mechanism of regulation of fluid balance in the body by the hormone ADH, which translates into water retention by the kidneys and the development of a state of hyponatremia.A simple and effective treatment is to restore blood volume by intravenous infusion (infusion) of balanced intravenous solutions, which helps to “turn off” the signal of ADH excretion.

The state of hyponatremia in endurance athletes, against the background of dehydration, is usually accompanied by hypoglycemia (drop in blood glucose levels) due to insufficient consumption of carbohydrates at a distance, since errors in drinking and nutrition at ultra-distances are usually hand in hand.

Compliance with the regime of fluid intake and food is extremely important when going through ultra-distances.

RECOMMENDATIONS.

As we can see, the state of hyponatremia can be caused by two completely opposite physiological conditions. Unfortunately, I do not have a universal answer for everyone to the questions: “How to avoid conditions of hyponatremia?” Everything is very individual and depends on many input factors, such as: the gender of the athlete, his age, the level of preparedness, the time spent on the distance, the pace of the distance, climatic conditions, altitude, etc.etc., etc.

Study your body, learn to listen to your body, gain experience. Increase your training and competition volumes gradually.

This is probably the only universal remedy for all problems.

Get to know yourself, gain experience, develop a drinking and nutrition regime that suits you. Do not try to surprise yourself and the world (which you can hardly surprise with something) by “feeling” the boundaries of your own capabilities. All these are extremely risky experiments on your own health, and you have one.You should not go out on a marathon distance with little running experience behind your back.

You can only enter the marathon distance if you have confidently and repeatedly covered a distance of 25 km and more during training. It is necessary to approach ultra distances from the marathon and longer with luggage from several marathons with good time (conventionally 3:30 for men and 3:45 for women). The increase in the competitive ultradistance should take place sequentially – a marathon, 50-60 kilometers, 70-80 kilometers, 100 kilometers and more.It is necessary to accumulate sufficient baggage of ultra-distances from 60-70 kilometers (at least 3-5 successful finishes) before approaching a distance of 100 kilometers.

When it comes to cross-country running, 50 kilometers on asphalt will not be the equivalent of 50 kilometers on rough terrain, and even with a climb. On a “smooth” distance of 50 kilometers, you conditionally spend 5-6 hours of running time, while on a trail distance of 50 kilometers, and even in the mountains with a climb of 2,000 meters, you can take from 8 to 10 hours of running time , that is, twice as much.This is a completely different mode of the body’s work.

Such a gradual increase in the competitive distance, supported by undoubtedly appropriate training volumes, will not only allow you to go to the start prepared, but also give you time to accumulate much-needed running experience, teach you to listen and feel your body.

Only the accumulated running experience, the ability to listen and feel your body, will allow you to develop your most effective, individual, water and nutritional regimen, which you can independently regulate depending on various factors during the course of the competition distance.

Material prepared in collaboration with Dr. Evgeny Suborov.


90,000 Volume wasting in adults – Symptoms, diagnosis and treatment

A decrease in fluid volume is characterized by a decrease in the volume of extracellular fluid that occurs due to a deterioration in water-salt balance on a permanent basis.

The most common etiologies are hemorrhage, vomiting, diarrhea, diuresis, or sequestration of fluid in the third space.

Taking a detailed history and careful medical examination are critical to determining the etiology.

Signs and symptoms may include: postural dizziness, fatigue, confusion, muscle cramps, chest pain, abdominal pain, postural hypotension, or tachycardia.

Clinical symptoms usually do not appear until large fluid loss occurs.

Without proper medical examination and timely resuscitation, severe dehydration can lead to acute vascular insufficiency and shock.

May be accompanied by electrolyte imbalance or acid-base imbalance.

In most cases, isotonic crystalloid is the best starting method for dehydration.

A decrease in fluid volume is characterized by a decrease in the volume of extracellular fluid, which occurs due to a deterioration in the water-salt balance on a permanent basis.[1] Mange K, Matsuura D, Cizman B, et al. Language guiding therapy: the case of dehydration versus volume depletion. Ann Intern Med. 1997 Nov 1; 127 (9): 848-53.
http://www.ncbi.nlm.nih.gov/pubmed/9382413?tool=bestpractice.com
[2] McGee S, Abernethy WB 3rd, Simel DL. The rational clinical examination: is this patient hypovolemic? JAMA. 1999 Mar 17; 281 (11): 1022-9.
http://www.ncbi.nlm.nih.gov/pubmed/10086438?tool=bestpractice.com
[3] Batlle D, Chen S, Haque S. Physiological principles in the clinical evaluation of electrolyte, water, and acid-base disorders.In: Alpern RJ, Caplan MJ, Moe OW, eds. Seldin and Giebisch’s the kidney: physiology and pathophysiology. 5th ed. San Diego, CA: Academic Press; 2012: 2477-512. It may result from renal failure (diuresis) or extrarenal lesions (gastrointestinal, respiratory, skin, fever, sepsis, or third space sequestration). [4] Di Somma S, Gori, CS, Grandi T, et al. Fluid assessment and management at the emergency department. Fluid overload diagnosis and management.Contrib Nephrol. 2010; 164: 227-36.
http://www.ncbi.nlm.nih.gov/pubmed/20428007?tool=bestpractice.com
Without proper medical examination and timely resuscitation, severe dehydration can lead to acute vascular collapse and shock. [5] Rose BD, Post TW. Hypovolemic states. In: Clinical physiology of acid-base and electrolyte disorders. 5th ed. New York, NY: McGraw-Hill; 2001: 415-46.

Dehydration and decreased volume of intercellular fluid are not the same concepts, although they can occur in a patient at the same time.While they are often used interchangeably, it is important to differentiate between the two. Dehydration implies a general lack of water in the body as one of the manifestations or an increase in sodium loss, followed by an increase in plasma tone, which usually leads to the clinical manifestations of hyponatremia. This type of hypertension implies intracellular water contraction, while volume depletion implies a decrease in blood volume. [6] Bhave G, Neilson EG. Volume depletion versus dehydration: how understanding the difference can guide therapy.Am J Kidney Dis. 2011 Aug; 58 (2): 302-9.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4096820/

http://www.ncbi.nlm.nih.gov/pubmed/21705120?tool=bestpractice.com
Symptoms of pure water loss arise from the effects of increased osmolality and convey cellular responses to hypertension: confusion, thirst, impaired sensory status, and, in extreme cases, coma or seizures. In contrast, the clinical symptoms of a decrease in fluid volume are the result of the hemodynamic effects of a decrease in intravascular volume and are usually not associated with neurological changes.

How dehydration affects your riding efficiency

The feeling of thirst does not come to you immediately. Thirst begins to be felt only after the body has already lost 2% of the total volume of water. And a bad ride is just the beginning of your problems if you’ve already gotten dehydrated while driving. If the condition worsens, you may experience severe muscle fatigue and mental inhibition.

How it happens

If you regularly ride a bike, you will probably want to know the basics of the science of dehydration: because during exercise, the body temperature rises, the body is cooled by sweating.First, your body expels water from your blood, which changes the volume of your blood plasma. But the amount of water that can be drawn from the blood is limited, since cardiovascular function must still be maintained for the brain and lungs to function. If dehydration picks up steam, your body begins to draw water from muscle cells to support vital organs – and that’s when the biggest problems begin. Seizures can set in, and when using a power meter, you can see your power drop exponentially.

If you’ve already gotten to this extreme, gulping sports drinks and water won’t immediately reverse dehydration. Since it takes some time for water to pass its way from the stomach into the blood, it turns out that you continue to dehydrate for a while. Between 3% and 5% dehydration, you will begin to experience cognitive distortion, not only will the level of stress from the perception of the environment increase, but also the reaction time and attention will decrease – something that causes great problems for cyclists.

When you reach a dehydration level of 10% of the total, you will feel mentally tired and physically exhausted, and perhaps even a little sick. If you don’t drink fluids quickly, your exercises will end quickly – and you risk, including tomorrow’s classes. With significant dehydration, muscle recovery is more difficult and takes longer.

Drink to stay hydrated

So how much should you drink during a bike ride? It is hard to say.The dehydration experts are divided into a few general guidelines, and everyone sweats differently. Plus, some sweat is saltier than others: if you constantly have to scrape off the white salt crystals after travel, you may need to pay more attention to your salt intake than your travel buddy, i.e. it is worth monitoring the electrolyte content of drinks.

However, a good rule of thumb is ~ 250 grams of water every 20 minutes.And if you are going to ride for more than an hour, you need to drink a liquid with an 8% carbohydrate content. Therefore, drinking sports drinks saturated with electrolytes, which have a carbohydrate content of 6-8%, promotes better and faster recovery of fluid levels. Active transport proteins in the intestinal tract move carbohydrates very quickly into the blood stream and water molecules very quickly move immediately behind these carbohydrates.

Fun Fact: If you’re looking to make your own sports drink at home, pure fruit juices diluted 1: 1 with water will have the same effect as a nearly perfect 6-8% carbohydrate drink solution – but make sure that you also get electrolytes such as sodium, potassium and magnesium.We suggest you try one of the drinks described in this article.

Advice on fluid replenishment before and after arrival

Even if you are going on a rather long trip, there is no need to carry a bucket of liquid and revel in it. In addition to drinking water regularly while traveling, you can also fight dehydration by replenishing fluids before you travel. Before your upcoming trip, drink 2 glasses of liquid 15 minutes before departure.And don’t worry about having to go out after the start of the ride: this urge is regulated by the adrenal gland, and it will happen whether you drink or not, our experts say, but at least you start with a full tank.

If you are constantly absorbing fluids, remember that your body may not always be able to handle large amounts of it. Hyponatremia – excessive hydration – happens when the cells in the body absorb too much water. These are undoubtedly rare cases, but they do happen.If not taken in time, hyponatremia can lead to death. Therefore, you should not drink simply for fear of dehydration.

Finally, continue drinking after the end of the trip. Ideally, you should weigh yourself before and after arrival (without clothes), and drink a liter of fluid for every kilogram of weight lost. However, since sodium levels are likely to be lowered post-workout, the risk of hyponatremia is increased, so be sure to drink / eat something that contains salt, be it a restorative meal or an electrolyte-rich drink.

90,000 Do you need eight cups of water a day?

Photo caption,

Bottled water manufacturers constantly talk about the dangers of dehydration

Drinking at least two liters of water a day is advice that can be heard everywhere.

But Dr. Chris van Tulleken wonders how much this recommendation is warranted.

Remember how advertisers remind you that even the slightest dehydration will greatly affect you, so you need to “support the body with isotonic super water” that they sell?

This all sounds very scientific, doesn’t it? A man in a white coat, an athlete in electrodes, etc.And it’s very easy to sell something like that – when you’re sweaty and hot it seems that it’s natural and necessary to replenish the lost fluid.

So, this year sports doctors from Australia performed a unique experiment, the description of which was published in the British Journal of Sports Medicine. It argues that the idea of ​​the body’s loss of water as a limitation of physical capabilities is fundamentally wrong.

Researchers wanted to understand what happens to cyclists after 3% of their body weight is cleared from their bodies in the form of sweat.

The results of the athletes’ efforts were assessed after: a) maximum fluid loss; b) recovery of 2% of lost fluid; c) after complete saturation with water.

So far, nothing unusual, but the difference in approach to this and other studies was that the athletes did not realize exactly how much fluid they were receiving: water was given to them intravenously.

This is especially important because we all have an extremely subtle psychological perception of how much water we drink.

And what then? No difference in results between those who fully regained their water levels and those who lost maximum moisture.

Researchers refer to themselves as an “anti-drinking movement for athletes” who hope to convey to athletes that they should not drink too much water, because in this case they are threatened with a dangerous condition – hyponatremia, in which the amount of sodium in the blood drops to critical levels.

Evolution and advertising

Perhaps you shouldn’t be so surprised at the result.Humans evolved by doing manual labor in extreme heat and drought conditions.

Photo caption,

Tea, coffee, alcohol and food can restore fluid loss in the body

So what remains for those of us who don’t cycle through the Western Australian deserts?

There is an inescapable idea that we should drink at least eight cups of water (two liters) a day, not counting other drinks and food.

Our brains are washed with positive ideas of healing with water from all ailments from headaches to colic in the intestines, and without it we will die in agony in a matter of days.

This is such an obvious logical leap: since the lack of water is bad, then its overcompensation for the body is what the doctor ordered.

Of course, water improves your skin, speeds up your thought processes, prevents kidney stones from forming, gives your urine a healthy shine and a light shade instead of the dark orange fetid liquid that it turns into if you do not drink at work or visit restroom for a long day at work.

So I found an article that reported all this and more.In it, a group of distinguished specialists from France and the United States supported the requirement to drink 2-3 liters of water per day.

In addition to listing the healing properties of water, the group of doctors also referred to an article claiming that drinking too much water increases the risk of bladder cancer, but only tap water.

And then a little footnote at the end of the article made it clear that this scientific journal publication was an appendix sponsored by a major mineral water producer.

Its authors received royalties. And here it is – the answer. This is not research, but marketing.

That is why we are discussing this: more and more drinking water does not get to us for free from the taps. It is sold to us by the same smart people who add bifidobacteria to yoghurts, although they may not be of much use.

And all the same corporate employees persistently instill in us that we need to drink at least two liters of water a day.

Drink how to breathe

So where did this figure come from, which no one dares to dispute?

Here is a grain of truth: not very physically overloaded inhabitants of the temperate zone of the planet really need 6-8 cups of water a day, but they can assimilate a significant part of this moisture from food, tea, coffee or alcohol.

Yes, beer and coffee do not drain a lot of fluid out of you, which was wittily written back in 1982 by beer-loving medical students who undertook to examine their own urine.

There is no evidence that adding eight cups of water to what you already drink will suddenly benefit you, quite the opposite.

But there is much more wonderful news: you, like any titled sportsman, do not need to worry about the amount of fluid you drink, because the body solves this problem “automatically”.

If you drink too much, you will have to go to the restroom more often. If you barely poured liquid into yourself, you will be tormented by thirst. All this is as natural as the number of breaths in and out.

So claiming that you need more water is like asking you to breathe more “for better oxygen delivery to your lungs.”

Like many things in life, the golden mean is important here.

DEHYDRATION (DEHYDRATION)

Our body is made up of about two thirds of water.We only need the total water level to drop by a few percent so that we feel dehydration (dehydration) – that is, that our body does not have enough water. Lack of water can eventually lead to internal problems such as kidney stones, liver, muscle and joint damage.

Having Crohn’s disease or ulcerative colitis (the two main forms of inflammatory bowel disease – IBD) can sometimes increase the risk of dehydration. This fact sheet looks at why it can happen and some ways to prevent and treat it.

What is dehydration?

We feel the symptoms of dehydration if there is not enough water in our body. This can happen due to a combination of several reasons, for example, we do not drink enough water, or we lose too much fluid from the body (for example, due to vomiting or diarrhea).

Dehydration is usually described as mild, moderate, or severe, depending on how much body weight is lost due to fluid loss.

  • Mild dehydration is a loss of 3-5% of your body weight.It carries few risks and can usually be addressed by replacing lost salts and fluids.
  • Moderate dehydration is a loss of 5-9% of body weight and is more severe. Moderate dehydration that is chronic (ongoing) can affect kidney function and can lead to kidney stones. This problem can be solved by replacing the lost salts and liquids.
  • Severe dehydration – loss of more than 10% of body weight due to fluid loss is a very serious problem requiring immediate treatment and can be fatal.The patient needs to go to the hospital and take IVs to recover the lost fluid.
    Dehydration can be a very serious problem for children as their lower body weight and size makes them more susceptible to fluid loss.

    What causes dehydration?

    Dehydration (dehydration) occurs when we lose more fluid than we take in. We lose fluid and salt throughout the day in sweat, tears, breath, urine, and feces. Usually, the water and salt content of what we eat and drink compensates for this loss – but we become dehydrated if the loss of fluids exceeds our intake.

    Our kidneys and intestines work together to control fluid levels in the body. The intestines absorb salt and water, while the kidneys regulate how much of this is lost in urine. If a large amount of fluid is lost due to diarrhea, then the kidneys will be unable to regulate the balance of salt and water. This means you may need extra salt as well as extra fluid.

    Can I be dehydrated?

    Dehydration may not necessarily be a problem for everyone with Crohn’s disease or ulcerative colitis.However, you are more likely to be dehydrated if:

  • You suffer from frequent or watery diarrhea
  • You are not drinking enough water because, for example, you feel nauseous or have lost your appetite due to illness
  • You are losing more water and salts through your skin than usual because you have excessive sweating. This could be, for example, during hot weather or exercise, or because you have a fever.
  • You have frequent urination.This can happen if you have uncontrolled diabetes, use too much caffeine, or use diuretics that increase the amount of urine you make.
  • You have drunk too much alcohol. Alcohol is a diuretic that increases the amount of urine you release.
  • You have gastroenteritis, a stomach or intestinal infection that can be caused by a virus or bacterial infection, or food poisoning.
  • Your colon has been removed.This affects your body’s ability to absorb fluids and electrolytes (basic salts such as potassium and sodium) from your diet.
  • You have an ileostomy (or stoma) because the exit from the ileostomy contains more water than normal stools. If your ileostomy has a high yield – loss of more than 1500 ml per day – you run the risk of dehydration.
  • You have very short bowels as a result of major surgery.
  • You have bile salt malabsorption. This can happen if you have Crohn’s disease in the ileum (lower part of the small intestine) or have had a resection in this area.
    How do I know if I have dehydration?

    One of the first signs of dehydration is thirst. Mild dehydration can also cause dry mouth, headaches, fatigue, and lack of energy. Fainting when standing is another common symptom. If you urinate less than three to four times a day and in small volumes, you are probably dehydrated. Another early sign of dehydration is urine that is darker yellow than usual. Dehydration can also cause constipation, which can be a problem for people with proctitis (inflammation in the rectum).

    If you think you may have a mild dehydration problem, one way to check this is to measure the amount of urine you release in 24 hours; it must be at least a liter.

    Signs of more severe dehydration (“moderate” rather than “mild”) include dizziness, muscle cramps, pale and dry skin, and sunken eyes. See your doctor if you have these symptoms.

    You may be severely dehydrated if, in addition to any of these symptoms, you are disoriented in space, your lips turn blue, and your breathing or pulse becomes fast.You may also feel irritated or tired. Severe dehydration is dangerous and you will need urgent medical treatment.

    What if I am dehydrated?

    To treat dehydration, you need to restore lost salts and fluids. But just drinking plain water may not be enough.

    For mild to moderate dehydration, you will need to increase your fluid intake and salt levels in your body. One way to do this is by drinking rehydration solutions, which are available over the counter over the counter.Also, as a short-term event, drinking sugary water (such as cola) and eating a salty snack such as a bag of chips can be effective. If that doesn’t work, or if you feel like you’re constantly feeling dehydrated, talk to your doctor. Your doctor may suggest that you prepare and drink a prescription oral rehydration solution, as you can see below.

    For more severe dehydration, or if you have an ileostomy or short bowel after surgery, you will likely need more salt than most rehydration solutions available in the pharmacy.

    One of the recipes for the home version of oral rehydration solution is as follows:

  • Table salt – 3.5 g (about 1 teaspoon with heap)
  • Sodium Bicarbonate (Baking Soda) – 2.5 g (approximately one teaspoon without top)
  • Glucose or Sugar – 20 g (approximately 6 teaspoons)
  • 1 liter of water. If possible, use soda and / or a fruity, low sugar flavor. Refrigerate and drink chilled.
    This oral rehydration solution tastes both salty and sweet, so some people find it unpalatable if they don’t add fruit flavor. The usual recommendation is to drink a full liter in one day, sipping it slowly to maximize the rehydration effect.

    It is especially important to consult your doctor before taking oral rehydration solution if you have diabetes. This is because this solution has a high sugar content and can raise blood sugar levels if consumed too quickly or in large quantities, more than one liter per day.You should also talk to your doctor before taking oral rehydration solution if:

  • Your ankles are swollen
  • You are taking a diuretic tablet that promotes the production of urine
  • You have kidney problems.
  • You are taking pills for heart or blood pressure problems.
    How can I stay hydrated?
  • The easiest way to stay hydrated is to make sure you are drinking enough water.To stay hydrated, the recommended fluid intake in the UK is two liters per day for women and two and a half liters for men. Water, other drinks and liquids from food can all contribute to this. However, the ideal amount will depend on the individual depending on age, activity level, and the number of sweat glands. As a guideline, aim for eight to ten medium-sized glasses of water per day. Pale yellow urine is a good sign that you are well hydrated.
  • Plan for situations where you may be more prone to dehydration – for example, when it is very hot or you are active, as you will lose more salt and water through your skin. Don’t wait until you feel thirsty before drinking extra water.
  • Drinks such as tea, coffee, and cola will also help, but because they contain caffeine, they are mild diuretics and will make you urinate more. Therefore, these drinks are somewhat less effective in rehydration.
  • Drink drinks slowly, do not swallow them quickly. This will help prevent excess air from entering your May system and causing discomfort afterwards.
  • A balanced diet that includes foods rich in essential body salts (sodium potassium) such as avocados and bananas can also help maintain electrolyte balance in your body.
  • Avoid drinking alcohol, which can lead to dehydration.
    If I increase my fluid intake, will it make my diarrhea worse?

    If you have Crohn’s disease or ulcerative colitis but have normal or near-normal bowel length, drinking more water should not make your diarrhea worse.This is because diarrhea is more caused by IBD activity rather than an inability to absorb fluid from the intestines. For the same reason, fluid restriction probably will not reduce diarrhea, but it may increase the likelihood that you are feeling irritated.

    Maintain hydration with stoma

    If you have a stoma, it is especially important to drink enough water to maintain adequate fluid levels in your body. You may also need to add extra salt to your diet and possibly take oral rehydration solutions.But, consult your doctor first.

    Oral rehydration solutions may be helpful if you have a short bowel or high-yield ileostomy, but under these conditions you may also need to limit your total fluid intake to stay hydrated. This is because too much plain water can cause the water to flush essential salts out of the small intestine. Because water is absorbed better with sugar and salt, the loss of these salts through the outlet of the stoma can lead to dehydration.Your doctor will tell you this is the case and can help you manage your overall diet and fluid intake.

    Hyponatremia (overhydration)

    Although much less common than dehydration, overconsumption of water occasionally can be harmful. Drinking too much plain water in a short period of time can dilute the salt level in the blood and imbalance the electrolyte balance in the body. Overhydration symptoms include nausea, vomiting, and headache.

    In severe cases, the brain may swell, causing confusion and seizures.

    Source: https: //www.crohnsandcolitis.org.uk/about-crohns-and-colitis/publications/dehydration? Fbclid = IwAR1rZrxwgLy8FOeJxhnB_xwkJglCYx5g5nfLoLTltrVFRIgqESVFC8a3Jyc

  • Krames Online – Discharge instructions after hyponatremia (pediatric)

    Your child has been diagnosed with hyponatremia. This is a low level of sodium in the blood. Sodium helps the body to function normally.A lack of sodium can cause health problems. Very low sodium levels can be fatal. Low sodium levels have many causes. In young children, this is usually caused by a mixture being diluted with water or given too much plain water to drink. In older children, it can be caused by drinking too much water, certain medications, dehydration, or severe burns. Diseases of the kidneys, heart and liver can also cause this. Preventing hyponatremia involves treating the condition that is causing low sodium levels.The following is the information you need to know about home care. Your healthcare professional may give you different instructions.

    Home care

    • Limit your child’s fluid intake as recommended.

    • Ask your healthcare provider to find the best way to replenish your child’s fluid after vomiting or diarrhea.

    • Have your child replenish fluids gently after exercise or activities that cause sweating.Give your child an electrolyte sports drink or another type of drink as recommended by your doctor.

    • Tell the doctor about all medicines your child is taking. This includes over-the-counter drugs and prescription drugs. Some of them can lower sodium levels.

    • Give your child all the medicines as prescribed.

    • Check your child’s sodium levels as often as recommended.This is very important if your child is taking a diuretic. It is a medicine that helps to flush water out of the body.

    Follow-up

    See or follow instructions from your pediatrician. Your child will need to be closely monitored.

    When to contact your doctor

    Call a doctor immediately if the child has any of the following symptoms:

    • bloating and swelling of the face and fingers;

    • nausea and vomiting;

    • fatigue;

    • fainting, dizziness, or lightheadedness;

    • confusion of consciousness;

    • muscle weakness, colic or cramps;

    • headache;

    • disorientation;

    • convulsive seizures.