| EM guidemap - Hypernatremia |
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- treatment of hypernatremia
- determining the likely cause of the hypernatremia if the etiology is not clinically apparent
- causes of hypernatremia
- causes of central diabetes insipidus
- causes of nephrogenic diabetes insipidus
- algorithm for determining the cause of the hypernatremia
- formulae for fluid replacement therapy in hypernatremia
| Introduction |
Hypernatremia is defined as a serum sodium > 145 mEq/L
- hypernatremia can be due to:-
- net loss of water and sodium from the body with inadequate water replacement (commonest cause)
- inadequate water intake
- increased water loss from the body
- increased sodium load
- hypernatremia most commonly results from a net loss of water and sodium from the body coupled with inadequate water intake
- the hypotonic fluid loss can be due to renal (osmotic diuresis or diuretics) or extra-renal (skin or GIT) causes
- because thirst is such a powerful driving force, inadequate voluntary water intake is only common at the extremes of life (eg. infants who cannot control their water intake, or elderly patients who cannot access water due to mental or physical disability), or when patients-of-any-age have a blunted thirst drive or an inability to access water due to altered mental status (coma, over-sedation or over-tranquillization)
Inadequate water intake is a universal prerequisite for the evolution of hypernatremia
(* hypernatremia due to indequate water intake is rarely seen in alert patients with a normal thirst mechanism + access to water + an ability to obtain and drink water)
Inadequate water intake
- hypernatremia is rarely due to inadequate water intake without net fluid losses
- primary hypodipsia results from destruction of the thirst centers in the hypothalamus
- causes of primary hypodipsia include:-
- primary and secondary hypothalamic tumors (50%)
- granulomatous diseases (20%)
- vascular abnormalities (15%)
- trauma and other causes (15%)
- secondary hypodipsia is due to an inability to respond to thirst signals due to altered mental status, or due to an impaired ability to access water as a result of underlying physical or mental handicaps (common in infants and the elderly)
Increased pure water loss
- increased pure water losses may be due to extra-renal causes (increased sweating, hyperventilation), or diabetes insipidus
- pure water loss due to diabetes insipidus results from decreased secretion of ADH due to diseases of the hypothalamus-pituatry axis (central diabetes insipidus) or decreased renal tubular responsiveness to ADH (nephrogenic diabetes insipidus)
Diabetes insipidus usually only produces hypernatremia if the patient has an associated problem of decreased water intake
(* see the appendix for a list of causes of central diabetes insipidus, and a list of causes of nephrogenic diabetes insipidus)
Increased sodium load
- hypernatremia from pure sodium overload is rare, and is seen in CPR with excessive sodium bicarbonate administration, inappropriate mixing of powdered infant formulas, dialysis against a high sodium dialysate, and when hypertonic saline is used as an abortifacient
Effects of hypernatremia
- hypernatremia results in cell dehydration and cell volume contraction as water leaves the intracellular compartment => the body cells compensate over a period of hours-days by generating idiogenic osmoles (mainly aminoacids) within the cells to prevent cell dehydration and cell shrinkage
- brain cell shrinkage causes the brain to pull away from the calvarium => tearing of bridging subdural vessels => intracranial hemorrhage
- the opposite phenomenon may occur when water is replaced too quickly
in patients with chronic hypernatremia => water enters the brain cells,
which have not yet got rid of the previously-generated idiogenic osmoles
=> iatrogenic brain edema
| Clinical presentation |
- common manifestations of hypernatremia are non-specific, and include restlessness, irritability, muscular twitching, hyperreflexia, spasticity, and seizures
- patients with hypotonic losses may present with signs of volume loss - tachycardia, hypotension, decreased JVP, dry mucosa, reduced skin turgor and thick doughy skin
- common symptoms in infants include hypernea, muscle weakness, restlessness, characteristic high-pitched cry, insomnia and lethargy
- the level of consciousness correlates with the level of hypernatremia;
however, muscle weakness, confusion and coma can be due to the underlying
co-existing condition
| Medical decision-making |
Managing hypernatremia requires a two-pronged aproach - addressing the underlying cause and correcting the hypernatremia
- the manner of addressing the underlying cause is cause-dependent, and may involve stopping GIT fluid losses, withholding lactulose or diuretics or lithium, treating hyperpyrexia or hyperglycemia .... etc.
- treatment of the hypernatremia depends on the underlying pathophysiological cause:-
- water and sodium loss
- pure water loss
- excess sodium administration
- a hypernatremic patient with water and sodium loss is usually clinically dehydrated +/- hemodynamically unstable => fluid therapy is first indicated to correct organ hypoperfusion, and IV 0.9 N/S should be administered until hemodynamic stability is ensured => 0.45 N/S is then used if the sodium loss is ongoing, or 5% D/W if the sodium loss has been halted (0.2 N/S is often used in children)
0.9 N/S should only be used to ensure hemodynamic stability, and a more hypotonic fluid should be substituted as soon as the state of hemodynamic instability has been corrected
Pure water loss (Euvolemic hypernatremia)
- the preferred route of fluid replacement is the oral route (or a feeding tube prn); suitable fluids include 5% D/W, or 0.2 N/S, or 0.45 N/S; the more dilute the fluid => the slower the rate of fluid administration
- 5% D/W is the fluid of choice for IV administration if there is no associated sodium deficit and secondary hypovolemia
- if one is unsure whether associated hypovolemia exists => measure the urine sodium
- low urine sodium < 10 mEq/L suggests hypovolemia => administer 0.45 N/S until the clinical signs of hypovolemia disappear, and the urine sodium is > 20 mEq/L
- urine sodium > 20 mEq/L in the context of diabetes insipidus => presume that the volume status is normal and administer 5% D/W as the fluid of choice
- in patients with diabetes insipidus and ongoing renal water losses => administer additional free water in addition to the calculated free water deficit, which is based on the serum sodium level
(* see the appendix for formulae that can be used to calculate the free water deficit, and the rate of fluid administration)
Excess sodium (Hypervolemic hypernatremia)
- treatment involves furosemide (1mg/kg) to get rid of sodium + free water replacement as 5% D/W
(* furosemide alone will aggravate the hypernatremia because a furosemide-induced diuresis is equal to one-half isotonic saline solution => electrolyte-free water needs to be administered in addition to furosemide)
- dialysis may be required for patients with oliguric renal failure
Rate of fluid replacement
Fluid therapy should be slow in patients with pure water loss, or combined water loss and sodium loss
- the total free water deficit should be corrected in 48 - 72 hours, especially if the hyponatremia is chronic (> 2 days), to minimize the risk of iatrogenic brain edema
- the rate of free water replacement should be calculated to decrease the free water deficit by 50% in 24 - 36 hours, and no faster than a 0.5 - 1mEq/L decrease in serum sodium per hour and a maximum decrease of 12 mEq/L in serum sodium/24 hours
- patients who develop acute hypervolemic hypernatremia within a few hours of an iatrogenic sodium load can be treated expeditiously, because the risk of brain edema is very small
Determining the likely cause of the hypernatremia if the etiology is not clinically apparent
- if the cause of the hypernatremia is not clinically obvious, then determining the volume status of the patient and measuring the urine osmolality and urine sodium may offer clinical clues as to the likely etiology of the hyponatremia
- if the patient is hypervolemic, the likely cause is sodium overload
- if the patient is hypovolemic, the likely cause is a renal or extra-renal cause of sodium and water loss producing a hypotonic fluid deficit
- urine sodium > 20 mEq/L + urine osmolality < 700 mOsm/kg => renal hypotonic fluid loss (eg. diuretics, osmotic diuresis)
- urine sodium < 10 mEq/L + urine osmolality > 700 mOsm/kg => extrarenal hypotonic fluid loss (eg. GIT or skin losses)
- urine osmolality < 700 mOsm/kg + polyuria => renal water loss due to diabetes insipidus
- urine osmolality > 700 mOsm/kg + oliguria => hypodipsia (or extra-renal pure water loss)
- if the cause of the diabetes insipidus is not clinically apparent, measuring baseline plasma vasopressin levels (which requires a reference laboratory) and/or assessing the kidney's concentrating ability in response to administered vasopressin may offer clinical clues => a low baseline plasma vasopressin level and an ability to concentrate the urine by > 50% following vasopressin administration (5 units of aqeous vasopressin sc or 10 mcg of dDVAVP intranasally) suggests central diabetes insipidus; a water deprivation test can also be used but it requires careful preparation and constant monitoring, and is not an ED procedure
(* see the algorithm
for determining the cause of the hypernatremia and the tables of causes
of central diabetes insipidus and nephrogenic
diabetes insipidus)
| Appendix |
Net water loss
Net pure water loss
Unreplaced insensible losses (dermal and respiratory)
Primary hypodipsia - due to hypothalamic thirst center lesions
Secondary hypodipsia - due to impaired perception of thirst, or inability
to access water
Neurogenic diabetes insipidus
Nephrogenic diabetes insipidus
Net hypotonic fluid loss
Renal causes
- loop diuretics
- osmotic diuresis
- post-obstructive diuresis
- polyuric phase of acute tubular necrosis
- intrinsic renal disease
- vomiting
- nasogastric drainage
- entero-cutaneous fistula
- diarrhea
- osmotic cathartic abuse
- burns
- excessive sweating
Hypertonic sodium bicarbonate infusion
Hypertonic feeding preparation
Ingestion of sodium chloride tablets
Salt used for gargling solution
Excessive use of baking soda as an antacid
Ingestion of sea water
Sodium chloride-rich emetics
Hypertonic saline enemas
Intrauterine injection of hypertonic saline
Hypertonic saline infusions
Mineralocorticoid excess (Cushing's syndrome and primary hyperaldosteronism)
Ticarcillin and carbenicillin (high doses)
| Causes of central diabetes insipidus |
| Head trauma
Post-surgical (hypophysectomy) Tumors
|
| Causes of nephrogenic diabetes insipidus |
| Congenital
Medications
Chronic tubulo-interstitial kidney diseases
|
Algorithm for determining the cause of the hypernatremia
Formulae for fluid replacement therapy in hypernatremia
Free water deficit
Free water deficit = 0.6 x body weight (kg) x [(plasma sodium /140) - 1]
- the free water deficit can be replaced rapidly in acute hypernatremia, which has developed over a few hours; however, it should be replaced slowly in chronic hypernatremia, which has developed over > 2 days (50% replacement in the first 24 hours, and complete replacement in 48 - 72 hours)
- free water replacement therapy should also take into account the degree of ongoing water loss and/or the balance of sodium and water in the ongoing fluid loss => the treating physician may choose to measure the serum sodium every few hours during the first 12 - 24 hours to ensure that the serum sodium does not decrease faster than 0.5 - 1.0 mEq/L/hour if he is not comfortable using formula to calculate the free water deficit and the precise rate of fluid administration
- maintenance fluid and electrolyte therapy to maintain urine output and replace insensible losses must also be given in addition to replacement of the free water deficit
Alternative formulae for fluid replacement
- the following approach has the advantage that it takes into account the effect of different concentrations of sodium and potassium in the infusate, and it allows one to re-calculate the fluid replacement rate whenever one changes the composition of the infusate solution
The formula is used to determine the effect of one litre of any infusate on the serum sodium
1) Formula for infusates containing sodium
Change in serum sodium = (infusate sodium - serum sodium) divided by (total body water + 1)
2) Formula for infusates containing sodium and potassium
Change in serum sodium = [(infusate sodium + infusate potassium) - serum sodium] divided by [total body water + 1]
Total body water = 0.6 x body weight (kg) for children and non-elderly
adult males, 0.5 x body weight (kg) for non-elderly adult females and elderly
males, 0.45 x body weight (kg) for elderly females
| Infusate | Infusate sodium (mmol/L) |
| 5% D/W | 0 |
| 0.2% sodium chloride in 5% D/W | 34 |
| 0.45% sodium chloride in water | 77 |
| 0.9% sodium chloride in water | 154 |
Practical example: A demented 70 year old nursing home patient, weighing 68 kg, presents to the ED with severe obtundation, fever, tachypnea, dry mucous membranes, decreased skin turgor and normal blood pressure. The serum sodium is 168 mEq/L. The diagnosis is pure water loss hypernatremia due to a combination of fever-induced hypernea and sweating + decreased water intake. The chosen therapeutic fluid is 5% D/W. The calculated total body water = 34 L (0.5 x 68).
Acccording to the formula, one litre of 5% D/W will reduce the serum sodium by 4.8 mEq/L
[* calculation = (0 - 168) divided by (34 + 1)]
If the goal of therapy is to reduce the serum sodium by 10 mEq/L over 24 hours, then 2.1 litres of 5% D/W is required
[* calculation = 10 divided by 4.8]
If 1.5L is the amount of maintenance fluid required for "average" obligatory water losses, then 3.6 L of 5% D/W is required over the first 24 hours (150 ml/hour)
Disclaimer: My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use.