Dehydration with hyponatremia: Hypernatremia and Hyponatremia: What Is the Difference?

05.09.202308.07.2023 by alexxlab

Hypernatremia and Hyponatremia: What Is the Difference?

Written by WebMD Editorial Contributors

What Is Dehydration?
Types of Dehydration
Treatment for Dehydration
When to Call a Doctor

It’s a well-known fact that the human body is more than 60% fluid. In addition to water, your bodily fluids contain vitamins, minerals, and other nutrients that keep the body functioning well. Sodium – an electrolyte – is a critical nutrient for all people. Everyone needs a certain amount of it in their bodies.‌

If the balance of fluids and sodium is upset, you can experience hypernatremia – having too much sodium and not enough fluid. Or you can experience hyponatremia – having too much fluid and not enough sodium. Both of these conditions can be the result of dehydration.

Dehydration is what happens when your body doesn’t have enough fluids to carry out all its normal functions. Your body needs a balance of water and enough of the nutrients known as electrolytes to work properly. If you dip below the ideal levels for either of those things, you can experience symptoms of dehydration.

You become dehydrated when you lose fluids and electrolytes, particularly sodium, but you don’t replace them by eating or drinking. Fluids leave your body through sweating, urination, and in the vapor that you breathe out from your lungs. You can lose fluids rapidly due to:

Diarrhea
Vomiting
Excessive sweating
Fever
As a side effect of some medications

When you lose a balanced combination of sodium and water, you experience isotonic dehydration. This means both your fluid levels and your sodium levels are lower than they should be. You will need to replace both fluids and sodium if this happens.

There are also cases where you can lose mainly fluid or mainly sodium. Losing mainly fluid is known as hypertonic dehydration – or hypernatremia. Losing mainly sodium is known as hypotonic dehydration – or hyponatremia.

Hypertonic dehydration (hypernatremia). Hypertonic dehydration happens when you lose water from your body but don’t lose an equal quantity of electrolytes, specifically sodium. You will have too high a sodium concentration in your blood and other bodily fluids. Typically, this causes you to feel thirsty, so that you want to drink water to replace the fluids you lost.

In some cases, you may be losing fluids faster than you can replace them. This may happen due to:‌

Vomiting
Diarrhea
Use of diuretics
Excessive sweating
Frequent urination due to high blood sugar
Kidney disease

If hypernatremia isn’t treated, you could experience worsening thirst. You could go on to develop confusion, muscle twitches, or seizures. In severe cases, hypernatremia can lead to coma and death.

Hypotonic dehydration (hyponatremia). Hyponatremia is what happens when you have too little sodium in your body. This can happen if you lose electrolytes and fluids together but only replace the lost fluids. It may happen if you drink only water and don’t take in other nutrients after losing a lot of fluids from sweating. Doing this will cause an imbalance of fluids and electrolytes.

Hyponatremia can also be the result of some diseases. Some causes of hyponatremia include:‌

Kidney failure
Heart failure
Liver cirrhosis
Use of diuretics
Certain medications, including chemotherapy drugs, anti-seizure medications, or anti-inflammatory drugs
Pancreatitis
Peritonitis
Addison’s disease

You might not feel thirsty if you are experiencing hyponatremia, because your fluid levels may be normal. Instead, the first symptoms of hyponatremia may be sluggishness and confusion. Without treatment, you may develop muscle twitches or seizures. Eventually, you could lapse into a coma or die.

Treatment for all types of dehydration involves replacing fluids and electrolytes in your body. In the case of mild dehydration, you can drink fluids that contain a combination of water and other ingredients to replace salt and other lost nutrients. Sports drinks or rehydration beverages with electrolytes are one option for rehydrating yourself. ‌

Another option is to drink water and eat a snack to get fluids and sodium into your body. Juice and soda may make diarrhea worse, so use caution in drinking those.

If you or another adult have the following symptoms of severe dehydration, you should seek medical attention:

Confusion
Dizziness
Infrequent urination
Dark-colored urine
Fatigue‌

Severe dehydration symptoms in young children and babies include:‌

Sunken soft spot on top of the skull
Irritable or listless
Dry mouth
No tears when crying
No wet diapers for 3 hours

A doctor will measure the sodium levels in your blood to determine what type of dehydration you have. Once they know that, they will give you fluids or an electrolyte solution. You may need to have this through an intravenous needle (IV) to speed up your recovery. ‌

Dehydration is a serious health issue. You can prevent dehydration by eating a balanced diet and drinking fluids, especially during exertion or hot weather. If you have underlying conditions that make you susceptible to dehydration, speak to your doctor about what you can do to stay safe.

Top Picks

Dehydration, Hypernatremia, and Hyponatremia – PubMed

Review

. 2015 Aug;31(3):389-99.

doi: 10. 1016/j.cger.2015.04.007.

Epub 2015 May 11.

John E Morley¹

Affiliations

Affiliation

¹ Divisions of Geriatric Medicine and Endocrinology, Saint Louis University School of Medicine, 1402 South Grand Boulevard, M238, St Louis, MO 63104, USA. Electronic address: [email protected].

PMID:
26195098
DOI:
10.1016/j.cger.2015.04.007

Review

John E Morley.

Clin Geriatr Med.

2015 Aug.

. 2015 Aug;31(3):389-99.

doi: 10. 1016/j.cger.2015.04.007.

Epub 2015 May 11.

Author

John E Morley¹

Affiliation

¹ Divisions of Geriatric Medicine and Endocrinology, Saint Louis University School of Medicine, 1402 South Grand Boulevard, M238, St Louis, MO 63104, USA. Electronic address: [email protected].

PMID:
26195098
DOI:
10.1016/j.cger.2015.04.007

Abstract

Disturbances of serum sodium are one of the most common findings in older persons. They are also a major cause of hospital admissions and delirium and are associated with frailty, falls, and hip fractures. Both hypernatremia and hyponatremia are potentially preventable. Treatment involves treating the underlying cause and restoring sodium and volume status to normal. The arginine vasopressin antagonists, vaptans, have increased the therapeutic armamentarium available to physicians.

Keywords:

Aging; Dehydration; Electrolytes; Hypernatremia; Hyponatremia; Osmolality; SIADH; Thirst.

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What is hyponatremia and how to avoid it

We have repeatedly mentioned the importance of drinking regimen during sports. The myth that you can’t take a sip of water during training has long been a thing of the past. On the contrary, more and more coaches and doctors are talking about how important it is to stay hydrated during heavy loads.

However, lack of fluid is not the only danger that threatens the long-distance runner. Along with sweat, we also lose salt, and then we exacerbate this process by pouring glass after glass of water on the run. This can lead to a significant reduction in plasma electrolytes and a dangerous state of hyponatremia.

What is this symptom and how to deal with it, we will describe in detail in this article.

Photo: Dina Rudick/Globe Staff

What is hyponatremia?

The term “hyponatremia” itself can be translated as “lack of sodium”, that is, in fact, salt deficiency. Sodium is the key electrolyte found in the intercellular space: it accounts for more than 60% of the total electrolytes. It is necessary in order to transmit impulses from muscle contraction and provide motor activity.

The normal concentration of sodium in human plasma is 135-145 mmol/l. With a slight decrease in these indicators, doctors diagnose a mild form of hyponatremia. The athlete may not even immediately understand that something is wrong with him. In the event that the plasma sodium concentration falls below 125 mmol / l, the symptoms become more pronounced and may require medical attention.

Types of hyponatremia

Depending on the concentration of electrolytes in the blood volume, hyponatremia is divided into three types:

Hypovolemia – insufficient volume of interstitial fluid, dehydration.
Hypervolemia – excess volume of fluid in relation to salts.
Euvolemia is a condition that develops at a normal concentration of sodium in the blood plasma due to an imbalance of the antidiuretic hormone.

For athletes, the first two types are most typical. The risk of hypervolemia during running occurs when an athlete consumes a lot of pure water or other unsalted drinks during the race. At the same time, minerals are excreted from the body along with sweat, and if you do not replenish their supply, then gradually the electrolyte balance in the body is disturbed.

Read on the topic: Isotonic: what is it for, how to choose and use it correctly

Hypovolemia has the opposite causes, but similar symptoms. Non-compliance with the drinking regimen in general and too little water consumed can lead to this condition.

Symptoms of hyponatremia

The severity of symptoms depends on the extent and speed of the fall in plasma sodium levels. Signs of hyponatremia in the initial stages: weakness, irritability, swelling of the extremities. Due to the decrease in concentration, the risk of stumbling and getting injured increases.

But these are all very non-specific signs, especially when it comes to endurance sports. Indeed, for ultramarathon runners, legs tangled from fatigue are a familiar phenomenon.

Experienced runners know that swollen fingers are already a dangerous symptom. This moment is easier to track and even feel if the rings begin to squeeze the skin unpleasantly. Also, scarce and rare excretion of fluid from the body should alert: this means that the kidneys cannot cope with the load.

Photo: trailrunplanet.com

If timely action is not taken, plasma sodium levels will continue to decline. Severe hyponatremia may be accompanied by convulsions, headaches, and vomiting. When the concentration of sodium ions decreases to 115 mmol / l, neurological problems that are life-threatening may occur.

Risk factors

Hyponatremia can affect any athlete, but there are several key risk factors:

Distance

The incidence of hyponatremia has increased more frequently in recent years as endurance sports become more popular. The longer the athlete is on the course, the more attention he needs to pay to electrolytic balance.

Hot weather

Together with sweat, we lose not only fluids, but also salt. When we are thirsty, we often drink more water than we need. And thereby further reduce the concentration of serum sodium.

Excessive or insufficient fluid intake

Dehydration at a distance leads to the same symptoms as excessive drinking: weakness, swelling of the limbs, dullness of attention.

Female gender

According to statistics, women suffer from hyponatremia more often than men. This may be due not only to hormonal characteristics. Even with the same body weight, the amount of intercellular fluid in the female body is less, so reducing its volume is more critical.

How to treat hyponatremia

If the serum sodium concentration has fallen slightly, then the intake of electrolytic solutions and even ordinary table salt will immediately improve the condition. A runner who suspects symptoms of hyponatremia may be helped by a glass of isotonic drink or a salty meal at the food station.

In acute and severe forms of hyponatremia, physicians use intravenous administration of a 3% NaCl solution in a volume of up to 150 ml in 20 minutes with a dropper. After that, the patient’s condition is assessed, and, if necessary, the procedure is repeated until the serum sodium concentration rises by at least 5 mmol / l.

After that, the treatment continues, but a less concentrated solution is used for droppers: only up to 0.9% NaCl. In this case, it is important not to rush, since a sharp increase in serum sodium for the patient is just as dangerous as a decrease.

How to avoid hyponatremia

To maintain the water-salt balance, it is recommended to monitor the level of electrolytes during heavy exercise. This is especially true in summer races during the heat, when sweating is especially active. In this case, it is better to drink often, but a little bit.

Instead of pure water, it is better to use an isotonic solution containing the required portion of electrolytes. Such a drink can not only be purchased at sports nutrition stores, but also prepared independently on the basis of ordinary table salt. A convenient option, especially for long races, will be salt tablets, which contain a concentrated portion of several minerals at once: sodium, potassium, magnesium and calcium.

Useful material: Salt tablets for running: what they are, how they work, when to use them

The organizers know what runners need, so food stations can also find something suitable to maintain electrolyte balance. Usually marathons offer salted peanuts or some snacks, and pickles are especially popular at Russian starts.

Although severe forms of hyponatremia are dangerous and require hospital treatment, the condition is not that difficult to prevent. The main thing is to be attentive to your feelings at a distance and not just hope to endure to the finish line on willpower.

Isotonics, saline tablets and electrolyte gels are not used by runners to splurge on trendy sports nutrition – they are really effective tools that will help to complete the distance without loss.

Read more: How much water should runners drink

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Hyponatremia: a clinical approach

AVP – arginine-vasopressin

MD – medicinal products

BMD – bone mineral density

SIADH – syndrome of inappropriate secretion of antidiuretic hormone

STN – salt-losing nephropathy

CHF – chronic heart failure

CNS – central nervous system

CP – liver cirrhosis

Abstract

Hyponatremia, defined as a decrease in serum sodium to 135 mmol/l or less, is the most common electrolyte disorder. The development of hyponatremia indicates a relative increase in the content of osmotically unbound water compared to the content of sodium in the body. This imbalance is a consequence of the excess consumption of osmotically free water over the ability of the renal tubules to dilute urine. In most cases, excess free water in the body is caused by increased secretion of the antidiuretic hormone, arginine-vasopressin (AVP), under the influence of osmotic and non-osmotic stimuli [1].

AVP is synthesized in the neurosecretory cells of the supraoptic and paraventricular nuclei of the hypothalamus, accumulates in the posterior pituitary gland and is released in response to an increase in blood plasma osmolarity. Even a small increase in plasma osmolarity (by 1%) causes the secretion of the hormone. AVP secretion is also regulated by non-osmotic stimuli. The concentration of AVP in the blood increases with a decrease in mean arterial pressure by 5–7% or a decrease in the effective volume of arterial circulation (“underfilling of the arterial bed”) by 8–10% [1, 2].

The effects of AVP are mediated by vasopressin receptors V1a, V1b and V2. Activation of V1a receptors in the vascular wall leads to systemic vasoconstriction. V1b receptors are predominantly located in the anterior pituitary gland. V2 receptors are localized mostly in the collecting ducts of the kidneys. When they are activated, a type 2 aquaporin free water channel protein moves to the apical surface of the latter, which increases the reabsorption of osmotically free water [3, 4].

The prevalence of hyponatremia in general therapeutic outpatient practice is not exactly known and, according to various sources, ranges from 21 to 34% [5-6]. In the elderly and in critically ill patients, the prevalence of hyponatremia is higher due to impaired urine dilution function and the ability to excrete osmotically free water.

Acute hyponatremia and, accordingly, a sharp decrease in extracellular osmolarity lead to an increase in intracranial pressure and the development of cerebral edema [7]. In the clinic of internal diseases, the so-called acute hyponatremic encephalopathy is an emergency situation, accompanied by high mortality (up to 42%). Concomitant hypoxia worsens the prognosis even more [8]. Chronic asymptomatic hyponatremia is also associated with a poor prognosis in hospitalized patients, including an increase in mortality and an increase in the length of stay in the hospital. At the same time, the prognosis is equally unfavorable, regardless of whether the patient arrives with hyponatremia or the latter develops during the hospital stay [9, 10]. The prevalence of hyponatremia in various conditions is presented in the table.

Prevalence of hyponatremia [13] Note. CHF – chronic heart failure.

Hyponatremia in the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). This is a clinical symptom complex in which excessive unregulated secretion of AVP leads to the development of hyponatremic overhydration. SIADH is the main cause of euvolemic hyponatremia – hyponatremia with normal volume of circulating blood, plasma and extracellular fluid. The diagnosis of SIADH requires the exclusion of hypervolemic hyponatremia in diseases accompanied by the development of edema (see below), and hypovolemic hyponatremia, which occurs with significant losses of water and sodium through the gastrointestinal tract (diarrhea, vomiting, loss to the “third space”) or kidneys (overdose diuretics, especially those acting distally, primary adrenal insufficiency, salt-losing nephropathy – STN, glucosuria in diabetes mellitus, bicarbonaturia with the development of metabolic alkalosis, salt-losing syndrome with damage to the central nervous system – CNS). Other causes of euvolemic hyponatremia are severe hypothyroidism and glucocorticoid deficiency in hypopituitarism. In these situations, hyponatremia is corrected by hormone replacement therapy [11, 12].

It is necessary to note the possibility of developing hyponatremia with suppressed AVP synthesis in the case of drinking a very large amount of liquid with limited salt intake (true water intoxication). With a daily osmotic load of 600 mOsm or more and suppressed AVP synthesis (normal state), electrolyte balance can be maintained at standard values when drinking up to 12 liters of liquid. Thus, in patients with primary psychogenic polydipsia, hyponatremia develops with the use of more than 12 liters of fluid per day. Limiting the osmotic load to 300 mOsm in the absence of APV secretion leads to the development of hyponatremia when 6 liters are consumed. This is how “beer sweating” develops, when, with a very large amount of beer drunk (hypoosmolar fluid) and insufficient intake of salts, hyponatremia occurs, despite the almost complete suppression of AVP synthesis and the maximum ability of the kidneys to dilute.

In patients with SIADH, hyponatremia develops with plasma hypoosmolarity and sufficient urine osmolality (more than 100 mOsm per 1 kg of water). In 10% of patients with hyponatremia and SIADH, diagnosed according to generally accepted criteria, the level of AVP in the blood cannot be determined. Probably, in these cases, the hormone is released at concentrations below the threshold of existing identification methods. Another explanation may be the development in these patients of nephrogenic SIADH associated with a mutation in the V2 receptor gene [13, 14].

The etiology of SIADH is diverse and includes a number of tumors, diseases of the central nervous system, lungs, the influence of drugs (LP), etc. The second most common cause of SIADH after tumors are diseases of the central nervous system. Any diffuse brain injury, including trauma, can lead to SIADH [15]. The latter can also develop with an exacerbation of almost any mental illness. At the same time, the nature of SIADH cannot be clarified in 40% of patients, especially the elderly [13].

LP-induced hyponatremia. L.P. is a common cause of hyponatremia. Hypovolemic hyponatremia due to the use of diuretics with severe dehydration develops quite rarely. However, distally acting diuretics and spironolactone can lead to the development of euvolemic hyponatremia associated with a violation of the concentration function of the tubules. Thiazide diuretics are a common cause of hyponatremia due to their widespread use. Other L.P. causing hyponatremia are presented below [16].

Drugs associated with hyponatremia (except thiazide diuretics):

AVP analogues: desmopressin, oxytocin.

Drugs that enhance the renal effect of AVP: chlorpropramide, cyclophosphamide, non-steroidal anti-inflammatory drugs, acetaminophen (paracetamol).

Drugs that increase the release of AVP in the pituitary gland: chlorpropamide, clofibrate, carbamazepine, vincristine, nicotine, opiates, ifosfamide;

Mechanism of hyponatremia unknown: haloperidol, fluphenazine, amitriptyline, thioridazine, fluoxetine, methamphetamine (ecstasy), sertraline.

Among them, the most common causes of hyponatremia are psychopharmacological drugs: carbamazepine, oxcarbamazepine and antidepressants from the group of selective serotonin reuptake inhibitors. Severe hyponatremia can develop with the use of drugs that act on the serotonin system (ecstasy, 3,4-methylenedioxymethamphetamine) [17].

Hyponatremia in cancer patients. About 14% of the causes of hyponatremia in hospitalized patients are malignant neoplasms [18]. In most cases, hyponatremia develops in patients with an established diagnosis of a tumor, but in some cases it precedes the detection of a neoplasm. In cancer patients, hyponatremia can complicate surgical or chemotherapy treatment, being an unfavorable prognostic factor in this category of patients [19].].

The main mechanism for the development of hyponatremia in malignant neoplasms is the ectopic production of AVP by the tumor, which leads to the development of SIADH. Most often, hyponatremia develops in lung cancer, especially small cell (in 10-15% of patients), as well as tumors of the head and neck. The latter are accompanied by the development of SIADH in about 3% of cases. At the same time, hyponatremia most often develops in patients with malignant neoplasms of the oral cavity, less often – of the pharynx, larynx, sinuses and salivary glands [20]. It is possible, however, the development of SIADH in tumors of other localizations.

The development of hyponatremia in cancer patients may complicate treatment with chemotherapy drugs, including vincristine, vinblastine, and cyclophosphamide [21]. The use of cisplatin and preparations based on it can lead to the development of STN, hypovolemia, and hypovolemic hyponatremia [22].

The use of large volume wound irrigation solutions for transurethral resection of the prostate or endometrial ablation can also cause transient hyponatremia [23].

Hyponatremia in the elderly. The prevalence of hyponatremia increases with age, as evidenced by its prevalence in patients in nursing homes, which is 18–22.5% [24, 25]. Most of these patients had at least one cause of hyponatremia, but in 7% of cases no clear cause could be identified. It should be noted that in the group of patients older than 75 years, hyponatremia was detected in 43% of cases, and all of them met the criteria for SIADH [24].

The true cause of hyponatremia in the elderly is unclear, but there are several hypotheses that explain this condition. It is likely that with age, a violation of sodium metabolism develops, close to SIADH [24]. Elderly patients have mild hyponatremia at baseline, but comorbidities or LP may exacerbate this, resulting in neurological symptoms. A certain contribution to the development of hyponatremia in patients of this category is also made by a decreasing feeling of thirst, which leads to hypovolemic hyponatremia [26].

Hyponatremia and fractures: imbalance and progression of osteoporosis. Chronic hyponatremia leads to the development of cognitive impairment, balance disorders and associated falls. In the presence of asymptomatic hyponatremia, the frequency of falls increases to 21.3% versus 5.4% in patients of the same age, but without impaired sodium metabolism [25].

The relationship between hyponatremia and decreased bone mineral density (BMD) has been studied in a number of studies. It is known that bones contain about 1/3 of all sodium reserves, and 40% of this sodium is able to enter the blood. In animal experiments, a decrease in BMD by 30% or more with prolonged hyponatremia has been demonstrated. It is likely that in chronic hyponatremia, sodium is activated from the bone tissue into the blood, which promotes the resorption of the bone matrix and bone demineralization [27]. Hyponatremia also increases the activity of osteoclasts, although the direct mechanism of this phenomenon is not well understood [28].

Hyponatremia with significant physical exertion. Hyponatremia can develop acutely during strenuous exercise, including in marathon, ultramarathon, and triathlon participants [29]. The prevalence of hyponatremia among amateur marathon runners is 3–13% [30–32]. A correlation was shown between the incidence of hyponatremia and an increase in body weight during the race, probably due to the unlimited use of drinking water, which is a hypoosmolar solution. There are also data on non-osmotic secretion of AVP during intense long-term exercise [33]. Risk factors for the development of hyponatremia in marathon participants are female gender, body mass index less than 20 kg/m ² and relatively low running speed in less trained athletes [30]. Acute severe hyponatremia can lead to severe neurological symptoms, including cerebral edema and seizures, neurogenic pulmonary edema, and even death.

Hyponatremia in CHF. The hypervolemic variant of hyponatremia is mainly found in CHF and liver cirrhosis (LC). The incidence of hyponatremia in decompensated CHF, according to some data, reaches 38% [9, 34]. The association of hyponatremia with an increase in total and cardiovascular mortality, as well as with repeated hospitalizations and low quality of life in these patients, has been demonstrated. In patients with CHF, in addition, the presence of hyponatremia increases the length of stay in the hospital and the risk of developing acute cardiorenal syndrome, and the adverse prognostic effect of hyponatremia persists even with long-term follow-up (4–5 years) [35, 36].

In CHF, hyponatremia develops despite plasma hypoosmolarity, in which AVP synthesis is normally maximally suppressed. The cause of hyponatremia in CHF is the non-osmotic secretion of AVP. In CHF, with a decrease in cardiac output, the stretching of baroreceptors in the wall of the aortic arch and carotid sinus decreases, which leads to disruption of the normal tonic inhibitory effect of the CNS mediated by the vagus and glossopharyngeal nerves [37]. The result is an increase in efferent sympathetic activity, which causes stimulation of the renin-angiotensin-aldosterone system and non-osmotic release of AVP [38].

The development of hyponatremia thus reflects an extremely dangerous combination of low cardiac output and maximum activation of neurohumoral systems, which is associated with a poor prognosis in many cardiac patients, including those with primary pulmonary hypertension, pulmonary embolism, and after cardiac surgery [39— 41].

Hyponatremia in cirrhosis. The main mechanism for the development of hyponatremia in cirrhosis is the non-osmotic secretion of AVP, caused by the “underfilling” of the arterial bed due to systemic (primarily intra-abdominal) vasodilation against the background of portal hypertension [42, 43]. Apparently, the main mechanism of vasodilation in cirrhosis is the effect of nitric oxide [44]. Hyponatremia in patients with cirrhosis is a predictor of hepatorenal syndrome and increases the risk of hepatic encephalopathy [45]. In a study of more than 500 patients with cirrhosis, hyponatremia was found to be a strong predictor of reduced quality of life and a worsening prognosis after liver transplantation [46–49].

Clinical approach for hyponatremia. The diagnostic algorithm in the presence of hypotonic hyponatremia is shown in the figure [50]. The use of this algorithm requires the exclusion of isotonic hyponatremia resulting from paraproteinemias, massive infusion of gamma globulins, the use of radiopaque agents, and severe hyperlipidemia (especially hypertriglyceridemia). Hyperosmolar conditions (hyperglycemia, mannitol infusion, significant positive anion gap) must also be ruled out. Thus, in all cases of hyponatremia, it is desirable to preliminarily determine the plasma osmolarity. Urinary osmolality in patients with hyponatremia usually exceeds 100 mOsm/kg. However, in patients with primary polydipsia and salt restriction (eg, beer sweating), urine osmolality may be low. It should be noted that pronounced natriuresis when taking diuretics can make it difficult to interpret indicators of urinary sodium excretion.

Clinical approach to the diagnosis and treatment of hyponatremia. AKI – acute renal failure; CRF – chronic renal failure.

The next step is to determine the total body fluid content. Diagnosis of hypervolemic hyponatremia is usually not very difficult due to the presence of signs of severe hypervolemia (edema, ascites) in severe CHF or cirrhosis. In clinical practice, infusion of saline (0.5–1 L for 12 h) helps to differentiate hypovolemic and euvolemic hyponatremia [51]. In SIADH, in most cases (especially with urine osmolality greater than 500 mOsm/kg), the injected sodium is rapidly excreted without changing the sodium content in the blood. At the same time, in hypovolemic hyponatremia, volume replacement normalizes sodium homeostasis in the blood. It should be emphasized that in euvolemic hyponatremia, in contrast to hypovolemic hyponatremia due to the absolute excess of osmotically free water, there are lower levels of uric acid, urea and creatinine in the blood. Moreover, the increase in uric acid excretion and decrease in its concentration in the blood in SIADH is not impaired even in the case of diuretics [52, 53].

The most reliable way to diagnose SIADH could be the determination of AVP in the blood. However, the complexity and high cost of the technique make it of little use in everyday clinical practice. In recent years, it has become possible to determine the content of copeptin in the blood, a stable glycopeptide formed from the precursor of AVP during the synthesis of the hormone in an equimolar ratio. Thus, the level of copeptin can indirectly indicate the content of AVP and differentiate primary polydipsia from SIADH [54].

If euvolemic hyponatremia, i.e. SIADH, is identified, the cause must be determined. First of all, the influence of a number of drugs, hypothyroidism and adrenal insufficiency should be rejected. The next step is to exclude the most common tumors leading to SIADH using computed tomography of the chest and magnetic resonance imaging of the brain. In some cases, especially in elderly patients, the genesis of SIADH cannot be established.

Therapy of hyponatremia. Treatment options for hyponatremia depend on the type (hypovolemic, hypervolemic, or euvolemic), duration, and severity of symptoms. Regardless of the cause of hyponatremia, severe neurological symptoms (convulsions, coma, respiratory arrest) require the immediate administration of 3% hypertonic sodium chloride solution to reduce the severity of cerebral edema. It is recommended to administer 100 ml of the solution as a bolus, if necessary, the administration can be repeated after 30 minutes [55]. Thus, the sodium content in the blood increases by 2-4 mmol/l. In rare cases, 200 ml of hypertonic saline is insufficient to achieve a clinical effect. The effect of hypertonic saline may enhance the simultaneous administration of furosemide. Successful use of 30-60 ml of 23.4% hypertonic sodium chloride solution for herniation of the brain stem caused by hyponatremia is described. Such a solution makes it possible to increase the level of sodium in the blood by more than 5 mmol/l [56].

Hypertonic sodium chloride solution must be prepared in a pharmacy and is rarely available. An 8.4% sodium bicarbonate solution can be used as a means for an emergency increase in the level of sodium in the blood. The osmolarity of 8.4% sodium bicarbonate solution is 2000 mOsm/l, which corresponds to the osmolarity of 5.8% sodium chloride solution. Thus, 50 ml of 8.4% sodium bicarbonate solution is equivalent to 100 ml of 3% sodium chloride solution in terms of increasing blood sodium levels.

With a rapid (within 24-48 hours) a significant decrease in the level of sodium in the blood, severe neurological symptoms develop. With a slower development of hyponatremia, “small” cerebral symptoms are noted: lethargy, disorientation, nausea, and impaired cognitive functions. In these cases, rapid progression to life-threatening conditions is possible, which also requires the use of hypertonic saline. At the same time, too rapid correction of hyponatremia is no less dangerous. Acute development of severe hyponatremia can lead to cerebral edema, however, with a longer exposure to electrolyte disorders (more than 48-72 hours), tissue adaptation occurs due to the diffusion of potassium and organic high-osmolar compounds (myrinositol, phosphocreatine) and amino acids (glutamine, taurine) from cells. In the latter case, a rapid increase in the level of sodium in the blood (more than 10–12 mmol/l/day) can lead to the development of a fatal complication of hypercorrection of hyponatremia — osmotic demyelination of the brain, which develops when the initial sodium level is less than 115–120 mmol/l [57, 58]. Risk factors for its development are concomitant severe liver disease, hypoxia, hypokalemia, cachexia, as well as an increase in the level of sodium in the blood of more than 25 mmol / l in 48 hours. Thus, the rate of correction of severe symptomatic hyponatremia should not exceed 10-12 mmol / l / days, and in patients with risk factors for the development of demyelination, chronic alcoholism and with an initial blood sodium level of less than 105 mmol/l – no more than 8 mmol/l/day [59].

Minimal neurological symptoms in hyponatremia: headache, decreased concentration, irritability, decreased mood and depression usually develop in patients with chronic electrolyte disturbances. In this situation, in addition to the treatment of the underlying disease, it is sufficient to limit fluid intake (with eu- and hypervolemic variant). The degree of restriction depends on diuresis. So, with a daily diuresis of 1200 ml, the daily fluid intake should not exceed 750 ml. With this restriction of fluid, an increase in the level of sodium in the blood by 1-2 mmol / l per day is noted. The effectiveness of fluid restriction is reduced with a higher ratio of urine osmolarity to plasma osmolarity [59].

In case of hypervolemic variants of hyponatremia (with CHF and cirrhosis), the basis of therapy is the use of large doses of loop diuretics with correction of hypokalemia and hypomagnesemia. The development of hyponatremia in these diseases reflects a decrease in “effective arterial blood flow”, severe disorders of central hemodynamics, and activation of neurohumoral systems. With decompensated CHF, the development of hyponatremia may be another reason for transferring the patient to the intensive care unit and prescribing intravenous inotropic drugs or vasodilators. With C.P. due to the increased risk of developing hepatorenal syndrome, the development of hyponatremia necessitates the infusion of albumin and colloids, the appointment of vasopressors in appropriate cases, as well as dose adjustment of lactulose, since the osmotic effect of the drug can reduce the amount of osmotically free fluid in the body and increase the level of sodium in the blood.

In order to correct hyponatremia, in addition to limiting fluid intake and the use of hypertonic solutions, in cases of developing CNS damage, it is possible to use demeclocycline, fludrocortisone, urea, as well as selective AVP receptor inhibitors, vaptans. Demeclocycline causes transient nephrogenic diabetes insipidus resistant to vasopressin, but the high toxicity of the drug limits its use in wide clinical practice [60].

Fludrocortisone is a mineralocorticoid hormone that enhances sodium absorption in the renal tubules. The use of this drug at a dose of 0.1-0.4 mg / day is the basis for the treatment of hyponatremia in adrenal insufficiency, as well as in salt-wasting syndrome with the development of hypovolemic hyponatremia, complicating brain damage. Successful use of the drug in SIADH against the background of small cell lung cancer has been described [61].

Osmotic diuresis with increased excretion of osmotically unbound water and, accordingly, correction of hyponatremia can be induced with the use of urea (15-30 g / day in divided doses). Successful use of urea through a nasogastric tube (0.5–1 g/kg/day) has been described in the intensive care unit [62]. A similar efficacy of urea and vasopressin receptor antagonists (vaptans) was shown during long-term use in patients with hyponatremia of various origins [63]. Another approach to the treatment of hyponatremia is to prescribe loop diuretics for increased salt intake.

Since most cases of hyponatremia are associated with the effect of AVP, blockade of its receptors by specific antagonists (vaptans) leads to the correction of electrolyte disturbances. The first drug from this group to find clinical use is conivaptan, a parenteral V1 and V2 receptor blocker [64]. The first oral V2 receptor blocker is tolvaptan. Long-term use (up to 3 years) of tolvaptan has been shown to be effective and safe; however, the first doses should be administered in a hospital setting to prevent too rapid an increase in sodium levels in the blood [65].

Hyponatremia is a frequent violation of electrolyte metabolism in the clinical practice of internists, nephrologists, oncologists, cardiologists, hepatologists, neurologists and resuscitators. Hyponatremia can accompany many diseases and is associated with their poor prognosis. At the same time, severe hyponatremia, regardless of the cause, can pose a threat to the patient’s life. Much less is known about the significance of chronic mild hyponatremia.

Approaches to the treatment of hyponatremia depend on the severity of neurological symptoms, its duration and type (hypo-, eu- or hypervolemic hyponatremia). In most cases (with the exception of the hypovolemic variant), hyponatremia reflects an excess of free water, and not a lack of sodium in the patient’s body as a result of a violation of the osmotic control system and osmotically independent secretion of ADH. The introduction of hypertonic sodium solution allows you to quickly eliminate the severe neurological manifestations of this electrolyte disorder. However, with long-term hyponatremia, therapeutic measures are aimed at suppressing the osmotically independent secretion of ADH or blocking the effect of ADH.

Dehydration with hyponatremia: Hypernatremia and Hyponatremia: What Is the Difference?

Hypernatremia and Hyponatremia: What Is the Difference?

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Dehydration, Hypernatremia, and Hyponatremia – PubMed

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What is hyponatremia and how to avoid it

What is hyponatremia?

Types of hyponatremia

Symptoms of hyponatremia

Risk factors

How to treat hyponatremia

How to avoid hyponatremia

Hyponatremia: a clinical approach

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