The human body relies on a complex system to maintain a delicate balance of sodium and water levels. Sodium, a dominant cation in extracellular fluid, is crucial in maintaining intravascular volume. The body’s ability to concentrate urine through the action of antidiuretic hormone (ADH) and increase fluid intake through a powerful thirst response are essential mechanisms to prevent the development of hypernatremia, defined as a serum sodium concentration of greater than 145 meq/L.
However, certain vulnerable populations and conditions can impair these protective mechanisms, resulting in vasopressin deficiency or unresponsiveness at the renal tubular level. Hypernatremia, if left untreated, can lead to serious complications such as altered mental status, seizures, and even death. Therefore, prompt diagnosis and treatment are crucial.
In addition to addressing the underlying cause of hypernatremia, treatment typically involves correcting the sodium imbalance through fluid replacement and medication. Overall, the body’s ability to maintain sodium and water homeostasis is a complex and delicate process involving various physiological mechanisms. Impairment of these mechanisms can result in serious health consequences, underscoring the importance of timely and appropriate diagnosis and treatment.
Epidemiology
Hypernatremia is commonly observed in two age groups, namely infants and the elderly population. Among infants, inadequate water replacement during episodes of gastroenteritis or ineffective breastfeeding are common scenarios that lead to hypernatremia. Moreover, premature infants are at higher risk due to their relatively small mass-to-surface area ratio and their dependency on caregivers to administer fluids. In addition, patients with neurological impairment are also prone to hypernatremia due to impaired thirst mechanisms and lack of water availability.
Hypernatremia is not only limited to infants and the elderly but can also occur in hospital settings. Hypertonic fluid infusions are one of the common causes of hypernatremia in the hospital setting, especially when combined with a patient’s inability to consume adequate water. In some cases, hypernatremia may also result from prolonged use of medications that affect water and electrolyte balance in the body, such as diuretics and lithium.
Anatomy
Pathophysiology
Sodium is an essential electrolyte that plays a crucial role in maintaining the balance of fluids in the body, particularly in the extracellular fluid (ECF) volume. Any deviation from the optimal sodium level can disrupt the ECF volume, leading to severe health complications. To maintain the sodium balance, the body employs an intricate feedback mechanism that increases or decreases sodium excretion in the urine.
This regulatory process ensures that the total sodium content remains constant within a narrow range. Several regulatory mechanisms are involved in sodium excretion, including the renin-angiotensin-aldosterone system. This system is activated when sodium levels in the body decrease, leading to the production of renin by the kidneys.
Renin then converts angiotensinogen to angiotensin I, which is subsequently converted to angiotensin II by the action of the angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that stimulates the release of aldosterone from the adrenal glands. Aldosterone acts on the kidneys, causing them to retain sodium and water and excrete potassium, helping restore the sodium balance.
When the serum sodium level increases, plasma osmolality increases, which triggers the thirst response and the secretion of antidiuretic hormone (ADH). The thirst response leads to an increase in water intake, while ADH acts on the kidneys to conserve water, producing concentrated urine. This process helps restore the body’s fluid balance, ensuring that the serum sodium levels remain within the normal range.
Etiology
The primary mechanisms that lead to hypernatremia are water deficit and excess solute. When the loss of total body water is greater than the loss of solutes, hypernatremia can occur. This imbalance is most commonly caused by combined water and solute loss, where the loss of water is greater than the loss of sodium. This can be seen in conditions such as vomiting, gastroenteritis, burns, prolonged nasogastric drainage, excessive sweating due to exercise, high heat exposure, or fever.
Hypovolemia is often associated with hypernatremia and can occur in conditions where both water and solute are lost. Renal losses can occur in intrinsic renal disease, post-obstructive diuresis, and using osmotic or loop diuretics. Hyperglycemia and mannitol are common causes of osmotic diuresis. Free water loss can occur in central or nephrogenic diabetes insipidus (DI) and conditions with increased insensible loss.
Central DI can occur due to inadequate antidiuretic hormone (ADH) production, commonly caused by head trauma, idiopathic cranial neoplasm, and pituitary infiltrative diseases such as histiocytosis and sarcoidosis. Nephrogenic DI occurs due to tubular unresponsiveness to the action of ADH and can be inherited in an X-linked pattern or secondary to certain medications, including lithium, foscarnet, and demeclocycline.
Inadequate fluid intake can also lead to hypernatremia, seen in breastfed babies, child or elder abuse, and patients with an impaired thirst response. On the other hand, excess sodium is usually iatrogenic and seen in the hospital setting but can also be associated with improper formula mixing, salt tablet poisoning, excess sodium bicarbonate ingestion, hyperaldosteronism, and seawater drowning.
Genetics
Prognostic Factors
Clinical History
Clinical History
Hypernatremia, a condition characterized by elevated serum sodium levels, can occur inside and outside the hospital setting. However, patients who develop hypernatremia outside the hospital are typically elderly and debilitated and often present with an acute illness such as fever. In contrast, hospital-acquired hypernatremia can affect patients of all ages. The clinician should take a thorough history to determine why the patient could not prevent hypernatremia with adequate oral fluid intake.
This includes identifying factors causing increased fluid excretion, such as fever, diuretic therapy, diabetes mellitus, diarrhea, and vomiting. The history should also cover symptoms and causes of possible diabetes insipidus, such as preexisting polydipsia or polyuria, a history of cerebral pathology, or medication use (such as lithium). It is important to determine whether the hypernatremia developed acutely or over time, as this information will guide treatment decisions.
Risk factors for hypernatremia include advanced age, mental or physical impairment, uncontrolled diabetes (leading to solute diuresis), underlying polyuria disorders, diuretic therapy, residency in a nursing home with inadequate nursing care, and hospitalization. Hospitalized patients may develop hypernatremia due to decreased levels of consciousness, tube feeding, hypertonic infusions, osmotic diuresis, lactulose, mechanical ventilation, or medication (such as diuretics or sedatives).
Physical Examination
Physical Examination
Patients with hypernatremia typically experience symptoms that suggest fluid loss and dehydration, and signs of dehydration are often clinically evident. When the serum sodium level rises rapidly or exceeds 160 meq/L, patients may experience symptoms and signs of central nervous system dysfunction. In infants and children, irritability and agitation are common initial symptoms, which can progress to lethargy, somnolence, and even coma. Other symptoms may include an increased thirst response in alert patients and a high-pitched cry in infants.
Patients with diabetes insipidus often present with polyuria (excessive urination) and polydipsia (excessive thirst). In addition, due to intracellular water loss, the skin may feel doughy or velvety. Hypovolemic hypernatremia is typically accompanied by orthostatic hypotension (a drop in blood pressure upon standing) and tachycardia (an increased heart rate). Patients may also exhibit increased tone with brisk reflexes and myoclonus.
It is important to note that in children with hypernatremia, dehydration can be underestimated due to a shift of water from the intracellular space to the extravascular space. Polyuria is one of the most common symptoms of diabetes insipidus, and it may be accompanied by polydipsia, which can lead to increased water intake and exacerbate hypernatremia. Therefore, it is crucial to identify and treat the underlying cause of hypernatremia to prevent further complications.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Cirrhosis
Central diabetes inspidus
Diarrhea
Hypocalcemia
Hyponatremia
Thirst defect
Nephrogenic diabetes insipidus
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
The first step in managing hypernatremia is to identify the underlying condition and correct the hypertonicity. The ultimate goal of therapy is to correct both the serum sodium and the intravascular volume. When managing hypernatremia, fluids should be administered orally or via a feeding tube whenever possible. However, the initial step in patients with severe dehydration or shock is fluid resuscitation with isotonic fluids before free water correction.
Calculating the free water deficit using one of the following formulas to correct hypernatremia is crucial. Remembering that rapid correction of hypernatremia can lead to cerebral edema, as water moves from the serum into the brain cells. Therefore, the goal is to decrease serum sodium by not more than 12 meq in 24 hours. Closely monitoring serum sodium every 2 to 4 hours is essential during the acute phase of correction.
If seizures occur during the correction of hypernatremia, it is a sign of cerebral edema due to rapid shifts in osmolality, and the administration of hypotonic fluids should be halted. The estimated free water deficit should be corrected over 48 to 72 hours with a decrease in serum sodium not exceeding 0.5 meq per hour. Patients should be carefully monitored for the rate of correction, urine output, and ongoing losses.
In some cases, such as sodium intoxication, the free water requirement may be too large and cause volume overload. In these cases, loop diuretics and peritoneal dialysis may be necessary to remove excess sodium. Desmopressin, available in intranasal and oral forms, may be required for older children and adults with central DI. However, it is crucial to note that water intoxication and hyponatremia are adverse effects seen with the use of desmopressin.
(off- label use)
For Chronic (>48 hours or unknown duration) as 5% dextrose solution:
Administer initial dose of approximately 1.35 mL/kg/hour intravenously up to a maximum of 150 ml/hour
For Acute (≤48 hours in duration) as 5% dextrose solution:
Administer initial dose of 3 to 6 mL/kg/hour intravenously up to a maximum of 666 ml/hour Dosing modification Renal impairment
No dose modification required Hepatic Impairment
No dose modification required
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The human body relies on a complex system to maintain a delicate balance of sodium and water levels. Sodium, a dominant cation in extracellular fluid, is crucial in maintaining intravascular volume. The body’s ability to concentrate urine through the action of antidiuretic hormone (ADH) and increase fluid intake through a powerful thirst response are essential mechanisms to prevent the development of hypernatremia, defined as a serum sodium concentration of greater than 145 meq/L.
However, certain vulnerable populations and conditions can impair these protective mechanisms, resulting in vasopressin deficiency or unresponsiveness at the renal tubular level. Hypernatremia, if left untreated, can lead to serious complications such as altered mental status, seizures, and even death. Therefore, prompt diagnosis and treatment are crucial.
In addition to addressing the underlying cause of hypernatremia, treatment typically involves correcting the sodium imbalance through fluid replacement and medication. Overall, the body’s ability to maintain sodium and water homeostasis is a complex and delicate process involving various physiological mechanisms. Impairment of these mechanisms can result in serious health consequences, underscoring the importance of timely and appropriate diagnosis and treatment.
Hypernatremia is commonly observed in two age groups, namely infants and the elderly population. Among infants, inadequate water replacement during episodes of gastroenteritis or ineffective breastfeeding are common scenarios that lead to hypernatremia. Moreover, premature infants are at higher risk due to their relatively small mass-to-surface area ratio and their dependency on caregivers to administer fluids. In addition, patients with neurological impairment are also prone to hypernatremia due to impaired thirst mechanisms and lack of water availability.
Hypernatremia is not only limited to infants and the elderly but can also occur in hospital settings. Hypertonic fluid infusions are one of the common causes of hypernatremia in the hospital setting, especially when combined with a patient’s inability to consume adequate water. In some cases, hypernatremia may also result from prolonged use of medications that affect water and electrolyte balance in the body, such as diuretics and lithium.
Sodium is an essential electrolyte that plays a crucial role in maintaining the balance of fluids in the body, particularly in the extracellular fluid (ECF) volume. Any deviation from the optimal sodium level can disrupt the ECF volume, leading to severe health complications. To maintain the sodium balance, the body employs an intricate feedback mechanism that increases or decreases sodium excretion in the urine.
This regulatory process ensures that the total sodium content remains constant within a narrow range. Several regulatory mechanisms are involved in sodium excretion, including the renin-angiotensin-aldosterone system. This system is activated when sodium levels in the body decrease, leading to the production of renin by the kidneys.
Renin then converts angiotensinogen to angiotensin I, which is subsequently converted to angiotensin II by the action of the angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that stimulates the release of aldosterone from the adrenal glands. Aldosterone acts on the kidneys, causing them to retain sodium and water and excrete potassium, helping restore the sodium balance.
When the serum sodium level increases, plasma osmolality increases, which triggers the thirst response and the secretion of antidiuretic hormone (ADH). The thirst response leads to an increase in water intake, while ADH acts on the kidneys to conserve water, producing concentrated urine. This process helps restore the body’s fluid balance, ensuring that the serum sodium levels remain within the normal range.
The primary mechanisms that lead to hypernatremia are water deficit and excess solute. When the loss of total body water is greater than the loss of solutes, hypernatremia can occur. This imbalance is most commonly caused by combined water and solute loss, where the loss of water is greater than the loss of sodium. This can be seen in conditions such as vomiting, gastroenteritis, burns, prolonged nasogastric drainage, excessive sweating due to exercise, high heat exposure, or fever.
Hypovolemia is often associated with hypernatremia and can occur in conditions where both water and solute are lost. Renal losses can occur in intrinsic renal disease, post-obstructive diuresis, and using osmotic or loop diuretics. Hyperglycemia and mannitol are common causes of osmotic diuresis. Free water loss can occur in central or nephrogenic diabetes insipidus (DI) and conditions with increased insensible loss.
Central DI can occur due to inadequate antidiuretic hormone (ADH) production, commonly caused by head trauma, idiopathic cranial neoplasm, and pituitary infiltrative diseases such as histiocytosis and sarcoidosis. Nephrogenic DI occurs due to tubular unresponsiveness to the action of ADH and can be inherited in an X-linked pattern or secondary to certain medications, including lithium, foscarnet, and demeclocycline.
Inadequate fluid intake can also lead to hypernatremia, seen in breastfed babies, child or elder abuse, and patients with an impaired thirst response. On the other hand, excess sodium is usually iatrogenic and seen in the hospital setting but can also be associated with improper formula mixing, salt tablet poisoning, excess sodium bicarbonate ingestion, hyperaldosteronism, and seawater drowning.
Clinical History
Hypernatremia, a condition characterized by elevated serum sodium levels, can occur inside and outside the hospital setting. However, patients who develop hypernatremia outside the hospital are typically elderly and debilitated and often present with an acute illness such as fever. In contrast, hospital-acquired hypernatremia can affect patients of all ages. The clinician should take a thorough history to determine why the patient could not prevent hypernatremia with adequate oral fluid intake.
This includes identifying factors causing increased fluid excretion, such as fever, diuretic therapy, diabetes mellitus, diarrhea, and vomiting. The history should also cover symptoms and causes of possible diabetes insipidus, such as preexisting polydipsia or polyuria, a history of cerebral pathology, or medication use (such as lithium). It is important to determine whether the hypernatremia developed acutely or over time, as this information will guide treatment decisions.
Risk factors for hypernatremia include advanced age, mental or physical impairment, uncontrolled diabetes (leading to solute diuresis), underlying polyuria disorders, diuretic therapy, residency in a nursing home with inadequate nursing care, and hospitalization. Hospitalized patients may develop hypernatremia due to decreased levels of consciousness, tube feeding, hypertonic infusions, osmotic diuresis, lactulose, mechanical ventilation, or medication (such as diuretics or sedatives).
Physical Examination
Patients with hypernatremia typically experience symptoms that suggest fluid loss and dehydration, and signs of dehydration are often clinically evident. When the serum sodium level rises rapidly or exceeds 160 meq/L, patients may experience symptoms and signs of central nervous system dysfunction. In infants and children, irritability and agitation are common initial symptoms, which can progress to lethargy, somnolence, and even coma. Other symptoms may include an increased thirst response in alert patients and a high-pitched cry in infants.
Patients with diabetes insipidus often present with polyuria (excessive urination) and polydipsia (excessive thirst). In addition, due to intracellular water loss, the skin may feel doughy or velvety. Hypovolemic hypernatremia is typically accompanied by orthostatic hypotension (a drop in blood pressure upon standing) and tachycardia (an increased heart rate). Patients may also exhibit increased tone with brisk reflexes and myoclonus.
It is important to note that in children with hypernatremia, dehydration can be underestimated due to a shift of water from the intracellular space to the extravascular space. Polyuria is one of the most common symptoms of diabetes insipidus, and it may be accompanied by polydipsia, which can lead to increased water intake and exacerbate hypernatremia. Therefore, it is crucial to identify and treat the underlying cause of hypernatremia to prevent further complications.
Differential Diagnoses
Cirrhosis
Central diabetes inspidus
Diarrhea
Hypocalcemia
Hyponatremia
Thirst defect
Nephrogenic diabetes insipidus
The first step in managing hypernatremia is to identify the underlying condition and correct the hypertonicity. The ultimate goal of therapy is to correct both the serum sodium and the intravascular volume. When managing hypernatremia, fluids should be administered orally or via a feeding tube whenever possible. However, the initial step in patients with severe dehydration or shock is fluid resuscitation with isotonic fluids before free water correction.
Calculating the free water deficit using one of the following formulas to correct hypernatremia is crucial. Remembering that rapid correction of hypernatremia can lead to cerebral edema, as water moves from the serum into the brain cells. Therefore, the goal is to decrease serum sodium by not more than 12 meq in 24 hours. Closely monitoring serum sodium every 2 to 4 hours is essential during the acute phase of correction.
If seizures occur during the correction of hypernatremia, it is a sign of cerebral edema due to rapid shifts in osmolality, and the administration of hypotonic fluids should be halted. The estimated free water deficit should be corrected over 48 to 72 hours with a decrease in serum sodium not exceeding 0.5 meq per hour. Patients should be carefully monitored for the rate of correction, urine output, and ongoing losses.
In some cases, such as sodium intoxication, the free water requirement may be too large and cause volume overload. In these cases, loop diuretics and peritoneal dialysis may be necessary to remove excess sodium. Desmopressin, available in intranasal and oral forms, may be required for older children and adults with central DI. However, it is crucial to note that water intoxication and hyponatremia are adverse effects seen with the use of desmopressin.
(off- label use)
For Chronic (>48 hours or unknown duration) as 5% dextrose solution:
Administer initial dose of approximately 1.35 mL/kg/hour intravenously up to a maximum of 150 ml/hour
For Acute (≤48 hours in duration) as 5% dextrose solution:
Administer initial dose of 3 to 6 mL/kg/hour intravenously up to a maximum of 666 ml/hour Dosing modification Renal impairment
No dose modification required Hepatic Impairment
No dose modification required
medtigo
Hypernatremia
Updated :
August 24, 2023
The human body relies on a complex system to maintain a delicate balance of sodium and water levels. Sodium, a dominant cation in extracellular fluid, is crucial in maintaining intravascular volume. The body’s ability to concentrate urine through the action of antidiuretic hormone (ADH) and increase fluid intake through a powerful thirst response are essential mechanisms to prevent the development of hypernatremia, defined as a serum sodium concentration of greater than 145 meq/L.
However, certain vulnerable populations and conditions can impair these protective mechanisms, resulting in vasopressin deficiency or unresponsiveness at the renal tubular level. Hypernatremia, if left untreated, can lead to serious complications such as altered mental status, seizures, and even death. Therefore, prompt diagnosis and treatment are crucial.
In addition to addressing the underlying cause of hypernatremia, treatment typically involves correcting the sodium imbalance through fluid replacement and medication. Overall, the body’s ability to maintain sodium and water homeostasis is a complex and delicate process involving various physiological mechanisms. Impairment of these mechanisms can result in serious health consequences, underscoring the importance of timely and appropriate diagnosis and treatment.
Hypernatremia is commonly observed in two age groups, namely infants and the elderly population. Among infants, inadequate water replacement during episodes of gastroenteritis or ineffective breastfeeding are common scenarios that lead to hypernatremia. Moreover, premature infants are at higher risk due to their relatively small mass-to-surface area ratio and their dependency on caregivers to administer fluids. In addition, patients with neurological impairment are also prone to hypernatremia due to impaired thirst mechanisms and lack of water availability.
Hypernatremia is not only limited to infants and the elderly but can also occur in hospital settings. Hypertonic fluid infusions are one of the common causes of hypernatremia in the hospital setting, especially when combined with a patient’s inability to consume adequate water. In some cases, hypernatremia may also result from prolonged use of medications that affect water and electrolyte balance in the body, such as diuretics and lithium.
Sodium is an essential electrolyte that plays a crucial role in maintaining the balance of fluids in the body, particularly in the extracellular fluid (ECF) volume. Any deviation from the optimal sodium level can disrupt the ECF volume, leading to severe health complications. To maintain the sodium balance, the body employs an intricate feedback mechanism that increases or decreases sodium excretion in the urine.
This regulatory process ensures that the total sodium content remains constant within a narrow range. Several regulatory mechanisms are involved in sodium excretion, including the renin-angiotensin-aldosterone system. This system is activated when sodium levels in the body decrease, leading to the production of renin by the kidneys.
Renin then converts angiotensinogen to angiotensin I, which is subsequently converted to angiotensin II by the action of the angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that stimulates the release of aldosterone from the adrenal glands. Aldosterone acts on the kidneys, causing them to retain sodium and water and excrete potassium, helping restore the sodium balance.
When the serum sodium level increases, plasma osmolality increases, which triggers the thirst response and the secretion of antidiuretic hormone (ADH). The thirst response leads to an increase in water intake, while ADH acts on the kidneys to conserve water, producing concentrated urine. This process helps restore the body’s fluid balance, ensuring that the serum sodium levels remain within the normal range.
The primary mechanisms that lead to hypernatremia are water deficit and excess solute. When the loss of total body water is greater than the loss of solutes, hypernatremia can occur. This imbalance is most commonly caused by combined water and solute loss, where the loss of water is greater than the loss of sodium. This can be seen in conditions such as vomiting, gastroenteritis, burns, prolonged nasogastric drainage, excessive sweating due to exercise, high heat exposure, or fever.
Hypovolemia is often associated with hypernatremia and can occur in conditions where both water and solute are lost. Renal losses can occur in intrinsic renal disease, post-obstructive diuresis, and using osmotic or loop diuretics. Hyperglycemia and mannitol are common causes of osmotic diuresis. Free water loss can occur in central or nephrogenic diabetes insipidus (DI) and conditions with increased insensible loss.
Central DI can occur due to inadequate antidiuretic hormone (ADH) production, commonly caused by head trauma, idiopathic cranial neoplasm, and pituitary infiltrative diseases such as histiocytosis and sarcoidosis. Nephrogenic DI occurs due to tubular unresponsiveness to the action of ADH and can be inherited in an X-linked pattern or secondary to certain medications, including lithium, foscarnet, and demeclocycline.
Inadequate fluid intake can also lead to hypernatremia, seen in breastfed babies, child or elder abuse, and patients with an impaired thirst response. On the other hand, excess sodium is usually iatrogenic and seen in the hospital setting but can also be associated with improper formula mixing, salt tablet poisoning, excess sodium bicarbonate ingestion, hyperaldosteronism, and seawater drowning.
Clinical History
Hypernatremia, a condition characterized by elevated serum sodium levels, can occur inside and outside the hospital setting. However, patients who develop hypernatremia outside the hospital are typically elderly and debilitated and often present with an acute illness such as fever. In contrast, hospital-acquired hypernatremia can affect patients of all ages. The clinician should take a thorough history to determine why the patient could not prevent hypernatremia with adequate oral fluid intake.
This includes identifying factors causing increased fluid excretion, such as fever, diuretic therapy, diabetes mellitus, diarrhea, and vomiting. The history should also cover symptoms and causes of possible diabetes insipidus, such as preexisting polydipsia or polyuria, a history of cerebral pathology, or medication use (such as lithium). It is important to determine whether the hypernatremia developed acutely or over time, as this information will guide treatment decisions.
Risk factors for hypernatremia include advanced age, mental or physical impairment, uncontrolled diabetes (leading to solute diuresis), underlying polyuria disorders, diuretic therapy, residency in a nursing home with inadequate nursing care, and hospitalization. Hospitalized patients may develop hypernatremia due to decreased levels of consciousness, tube feeding, hypertonic infusions, osmotic diuresis, lactulose, mechanical ventilation, or medication (such as diuretics or sedatives).
Physical Examination
Patients with hypernatremia typically experience symptoms that suggest fluid loss and dehydration, and signs of dehydration are often clinically evident. When the serum sodium level rises rapidly or exceeds 160 meq/L, patients may experience symptoms and signs of central nervous system dysfunction. In infants and children, irritability and agitation are common initial symptoms, which can progress to lethargy, somnolence, and even coma. Other symptoms may include an increased thirst response in alert patients and a high-pitched cry in infants.
Patients with diabetes insipidus often present with polyuria (excessive urination) and polydipsia (excessive thirst). In addition, due to intracellular water loss, the skin may feel doughy or velvety. Hypovolemic hypernatremia is typically accompanied by orthostatic hypotension (a drop in blood pressure upon standing) and tachycardia (an increased heart rate). Patients may also exhibit increased tone with brisk reflexes and myoclonus.
It is important to note that in children with hypernatremia, dehydration can be underestimated due to a shift of water from the intracellular space to the extravascular space. Polyuria is one of the most common symptoms of diabetes insipidus, and it may be accompanied by polydipsia, which can lead to increased water intake and exacerbate hypernatremia. Therefore, it is crucial to identify and treat the underlying cause of hypernatremia to prevent further complications.
Differential Diagnoses
Cirrhosis
Central diabetes inspidus
Diarrhea
Hypocalcemia
Hyponatremia
Thirst defect
Nephrogenic diabetes insipidus
The first step in managing hypernatremia is to identify the underlying condition and correct the hypertonicity. The ultimate goal of therapy is to correct both the serum sodium and the intravascular volume. When managing hypernatremia, fluids should be administered orally or via a feeding tube whenever possible. However, the initial step in patients with severe dehydration or shock is fluid resuscitation with isotonic fluids before free water correction.
Calculating the free water deficit using one of the following formulas to correct hypernatremia is crucial. Remembering that rapid correction of hypernatremia can lead to cerebral edema, as water moves from the serum into the brain cells. Therefore, the goal is to decrease serum sodium by not more than 12 meq in 24 hours. Closely monitoring serum sodium every 2 to 4 hours is essential during the acute phase of correction.
If seizures occur during the correction of hypernatremia, it is a sign of cerebral edema due to rapid shifts in osmolality, and the administration of hypotonic fluids should be halted. The estimated free water deficit should be corrected over 48 to 72 hours with a decrease in serum sodium not exceeding 0.5 meq per hour. Patients should be carefully monitored for the rate of correction, urine output, and ongoing losses.
In some cases, such as sodium intoxication, the free water requirement may be too large and cause volume overload. In these cases, loop diuretics and peritoneal dialysis may be necessary to remove excess sodium. Desmopressin, available in intranasal and oral forms, may be required for older children and adults with central DI. However, it is crucial to note that water intoxication and hyponatremia are adverse effects seen with the use of desmopressin.
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