Dehydration Hyponatremia: Causes, Signs, Symptoms, and Treatment

05.02.197923.11.2021 by alexxlab

What are the causes of dehydration hyponatremia? How do you recognize the signs and symptoms of low sodium levels? What is the best treatment for dehydration hyponatremia?

Содержание

Understanding Dehydration Hyponatremia

Hyponatremia, or low sodium levels in the blood, is a common condition that can occur in both hospitalized patients and outpatients. Its causes are numerous and can be challenging to pinpoint. However, having a straightforward approach to assessing and treating hyponatremia can be helpful in most cases encountered in clinical practice.

Diagnosing Hyponatremia

The symptoms and signs of hyponatremia can range from subtle to severe, but none are specific. The diagnosis is confirmed through laboratory findings, with hyponatremia typically defined as a serum sodium concentration of less than 134 mmol/L.

It’s important to note that hyponatremia can occur without being symptomatic, such as in cases of severe hyperglycemia or mannitol infusion, where the lowered serum sodium concentration is due to dilution by osmotic shifts of water out of cells. In these cases, the high serum osmolality helps differentiate these causes from other “true” causes of hyponatremia.

Causes of Dehydration Hyponatremia

True hyponatremia occurs when the serum osmolality or tonicity is decreased, indicating an inability of the body to excrete free water through the kidneys despite continued water intake. This can occur in the following three settings:

Contracted Extracellular Fluid (ECF) Volume

With ECF volume contraction from any cause (e.g., diarrhea, vomiting, excessive sweating, diuretic use), the release of antidiuretic hormone (ADH) is stimulated to defend ECF volume, making the kidney’s distal tubules more permeable to water reabsorption. Renin is also released in response to decreased renal perfusion, signaling 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.

Normal or Near-Normal ECF Volume

Expanded ECF Volume

Hyponatremia can also occur in the setting of expanded ECF volume, such as in congestive heart failure, liver cirrhosis, or nephrotic syndrome. In these conditions, there is a relative reduction in effective arterial blood volume, which stimulates the release of ADH and leads to water retention and hyponatremia.

Treating Dehydration Hyponatremia

The approach to treating hyponatremia depends on the underlying cause and the severity of the patient’s symptoms. When symptoms are mild, a conservative management approach aimed at removing the offending cause is often appropriate. However, when symptoms are severe, more aggressive correction of the serum sodium concentration, typically with intravenous therapy in the inpatient setting, may be necessary.

Case Study: Approach to Hyponatremia

In the case of the 72-year-old woman with a history of hydrochlorothiazide use, viral gastroenteritis, and symptoms of presyncope, the approach would be as follows:

The patient has a contracted ECF volume, as evidenced by the low jugular venous pressure and drop in blood pressure upon standing. The hyponatremia is likely due to the combination of diuretic use and the recent bout of gastroenteritis with diarrhea, leading to both sodium and water loss. The low urine sodium concentration (< 20 mmol/L) and low urine volume support this diagnosis.

The treatment in this case would focus on addressing the underlying cause of the ECF volume contraction. This may include temporarily discontinuing the hydrochlorothiazide, replacing fluids and electrolytes, and potentially administering intravenous saline if the hyponatremia is severe enough to be causing significant symptoms.

Conclusion

Dehydration hyponatremia is a common and complex condition, but a systematic approach to diagnosis and treatment can be helpful in most cases. Understanding the underlying causes, recognizing the signs and symptoms, and tailoring the management strategy to the individual patient are key to effectively addressing this electrolyte imbalance.

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)

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

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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.

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

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

Hyponatremia is the most common electrolyte abnormality in hospitalized patients.

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.

Evaluation of hyponatremia involves assessment of volume status.

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

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

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.

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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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.

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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?

October 10, 2013

Updated October 11, 2013

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.