- 1 Hypernatremia Definition
- 2 Hypernatremia Epidemiology
- 3 Hypernatremia Pathophysiology
- 4 Hypernatremia Causes
- 5 Hypernatremia Algorithm
- 6 Hypernatremia calculator
- 7 Hypernatremia Risk factors
- 8 Hypernatremia Symptoms
- 9 Hypernatremia Diagnosis
- 10 Hypernatremia treatment
- 11 Hypernatremia Correction
- 12 Hypernatremia Complications
- 13 Hypernatremia Prognosis
- 14 Hypernatremia Prevention
Hypernatremia is an imbalance in electrolyte, where the sodium level gets elevated in the blood. Generally, hypernatremia do not occur due to excess sodium; instead, it is caused due to free water deficiency in the body, which causes the sodium in the body to rise. Hence, hypernatremia is a water-problem rather than sodium homeostasis.
Hypernatremia due to excess salt intake is rare, and may happen in situations like salt water ingestion. Thus, hypernatremia is synonymous with dehydration. A strong thirst sensation resulting as a consequence of increased sodium level indicates hypernatremia, and this can be corrected by drinking water while feeling thirsty.
- Normal range: 136-145 mEq/L
- Hypernatremia: 145 mEq/L
- Severe hypernatremia: 152 mEq/L (seizures and even death can occur)
Reasons for water loss in the body
- Breathing (insensible losses)
- Urination and defecation
Hypernatremia is seen in around 1% of the hospitalized patients, as this condition usually is seen after hospital admission. Nearly 2% incidence is reported in breastfed infants and chronically ill elderly persons.
In the developing nations, pediatric patients are susceptible to hypernatremia due to infant feeding that may be made worse by poor production of maternal milk, secondary to nutritional deficiency, and errors in powdered formula reconstitution.
Hypernatremia has high mortality rate, especially elderly patients. Mortality rates are 42-75% in acute changes, and ranging from 10 to 60% in chronic hypernatremia. As hypernatremia is often associated with several other serious comorbidities, precise evaluation of the mortality degree occurring directly from hypernatremia is difficult. Morbidity in patient coping with hypernatremia is high, as many patients suffer from complications like permanent neurologic deficits.
Deaths result due to comorbidities, rather than hypernatremia alone. However, delay or inadequacy in treatment may increase the mortality rate. Persistent hypernatremia along with protracted hypotension in hospitalized patients has very poor prognosis.
Both genders are equally affected
Usually elderly individuals and breastfed infants (neonates)
Hypernatremia occurs when there is loss of water or hypertonic Na gain, and contains very little water compared to the total potassium and sodium. As the definition states, hypernatremia is a hyperosmolality state, where Na is the dominant cation and solute (extracellular).
Since the normal plasma osmolality ranges between 275-290 mOsm/kg, it is determined by the sodium salts’ concentration. Hence, the plasma osmolality regulation and sodium concentration in plasma is mediated by alteration in water intake and excretion.
This occurs via two mechanisms :-
- Urinary concentration (through pituitary secretion and effects of arginine vasopressin (antidiuretic hormone) in the kidneys.
Normally, thirst is stimulated when the fluid osmolality of the body increases above a certain threshold, resulting in an increased water intake, which rapidly corrects the hypernatremia
This mechanism is very effective. In conditions, where patients are not able to form urine concentration, as in diabetes insipidus and excess urine excretion of around 10 to 15 L/day, hypernatremia may not be caused, as thirst sensation is stimulated and osmolality of body fluid is also maintained, but with persisting secondary polydipsia. Hence, sustained hypernatremia will only be seen in impaired thirst mechanism, and intake of water does not increase due to the hyperosmolality, or in cases of restricted water intake.
Hypernatremia associated with euvolemia causes a decrease in TBW along with near-normal Na level of the body (or else, pure water deficiency). Extra-renal water loss, caused due to excessive sweating, thereby result in certain amount of sodium loss; however, as sweat is hypotonic, increased sodium levels can be caused before indicative hypovolemia occurs. Deficiency of water (pure) also results in central as well as nephrogenic diabetes insipidus.
Essential hypernatremia or primary hypodipsia seldom occurs in children suffering from brain damage, also in elderly adults with chronic illness. It is represented by a thirst mechanism that is impaired; this may be due to lesions in the thirst center of brain.
Alteration in the osmotic triggering for ADH release may be another possibility of euvolemic hypernatremia. There are some lesions causing both altered osmotic trigger and impaired thirst mechanism. Generally, patients are euvolemic, yet they have an intact non-osmotic release.
In rare cases, hypernatremia is related to volume overload. In such cases, hypernatremia occurs as a result of grossly elevated sodium intake in association with limited accessibility to water. For instance, excessive hypertonic NaHCO3 administration while treating lactic acidosis. It can also result as a consequence of hypertonic saline administration or due to improperly formulated hyper alimentation.
- Inadequate water intake, especially in elderly or disabled patients, for whom, water is not obtained even after thirst dictation. This is the most common reason for hypernatremia.
- Excessive water loss from the urinary tract that may be due to glycosuria, or various other osmotic diuretics.
- Extreme sweating.
- Severe diarrhea (watery)
Hypernatremia in elderly
Hypernatremia is very common amongst the elderly people, postoperative patients in particular, and also patients on tube feedings (parenteral nutrition). Apart from this, the following factors contribute to hypernatremia in elderly:
- Dependency in obtaining water
- Ineffective Thirst mechanism
- Ineffective renal concentrating capacity. This may be due to diuretics, or nephron loss associated with aging or renal conditions, impaired ADH release
- Impaired production of angiotensin II that may contribute in impairing the thirst mechanism.
Hypernatremia can result due to:-
- Net loss of both water and sodium content from the body along with inadequate water replacement
- Increased body’s water loss (renal or extra-renal)
- Inadequacy of water intake (universal prerequisite)
- Increment in the sodium load
- Insensible water loss = 500 to 1500 cc/day.
- Fever causes an increase in insensible water losses by 10% per degree Celsius when above 38° Or 100 to150 cc/day increment per degree Celsius when above 37°.
Hypernatremia Risk factors
- Elderly patients suffering from diseases associated with febrile illness.
- Infants with inadequate breast-feeding and diarrhea. An inexperienced mother or poor milk supply may be the cause of inadequate breast-feeding.
- Patients having altered mental status.
- Hypothalamic lesions, where the sense of thirst is affected (adipsia)
- Uncontrolled diabetes (solute diuresis)
- Diuretic therapy
- Underlying polyuria
- Inadequate nursing care
- Decreased consciousness level
- Hypertonic infusions
- Tube feeding
- Osmotic diuresis
- Medication like diuretics and sedatives
- Mechanical ventilation
- Lethargy and weakness
This mainly results from the acute plasma sodium concentration elevation more than 158 mEq/L. It also has high mortality rate.
- Neuromuscular excitability
- Cerebrovascular damage (Subarachnoid hemorrhage)
- Venous thrombosis
- Serum electrolytes (Na+, Ca2+, K+)
- Glucose level
- Lithium levels
- Plasma and urine osmolality
- Urine electrolytes (K+, Na+)
- 24-hour urine quantity or volume
- Plasma AVP level (only if indicated)
This is done to distinguish between nephrogenic and cntral diabetes insipidus. Hence, initially a Plasma AVP is taken, and then, the response of the osmolality of urine to an AVP dose is determined. In general,
- Osmolality increase> 50% – central diabetes insipidus
- Osmolality increase< 10% – nephrogenic diabetes insipidus Osmolality increase> 10- 50% – intermediate
- Hyperosmolar patients + elevated AVP level – nephrogenic diabetes insipidus
- Hyperosmolar patients + low AVP level – central diabetes insipidus
The first step for diagnosing hypernatremia is to assume the volume status (intravascular volume) in the hypernatremia patient. The volume contraction associated with it may be seen in a low amount of Na+ in urine (< 10 mEq/L).
In case of hypovolemia, urine with hyper-tonicity having UNa+ less than 10 mEq/L denotes fluid losses (extra-renal), as in cases of GI and dermal causes, whereas, an hypotonic or isotonic urine having UNa+ greater than 20 mEq/L represents renal fluid loss due to diuretics, intrinsic renal disease and osmotic diuresis.
In case of euvolemic with a preserved intravascular volume, elevated sodium level is mostly due to loss of pure-water. Normally, in hypernatremia, osmolality of urine should be concentrated to a maximum extent (greater than 800 mOsm/kg H2 O). Measuring the urine osmolality allows differentiation of the below-mentioned conditions.
- Non-renal causes associated with high urine osmolality- this causes Isolated hypodipsia.
- Renal water loss associated with low urine osmolality – this causes Diabetes insipidus (central, partial, nephrogenic and gestational diabetes insipidus), often Uosm less than 300 mOsm/kg H2 O
CT or MRI scan may be useful in conditions like central diabetes insipidus resulting from infiltrative lesions or head trauma. Histology It may be helpful in central diabetes insipidus.
- Diabetes Mellitus, Type 1
Treatment goals are as follows:-
- Treat any fundamental or cardinal disorder.
- Correct dehydration by the replacement of the lost free water.
- To correct hypovolemia if exists, by providing electrolytes along with free water.
This is done by:-
- Repeating the blood tests for confirming the true results, thereby excluding pseudo hypernatremia that maybe caused along with hypoproteinaemia, and also few serum sodium measuring techniques.
- Establishing, whether hypernatremia is acute, rapidly changing, stable or chronic. For determining hypernatremia, establishment of the foresaid states and clinical condition of the patient is very important, rather than the complete sodium content in the blood.
- Seeking specialist advice, when cause is non-proven still or there is no probability of oral rehydration, or sodium in blood is ≥ 155 millimoles/liter
To lower the sodium in blood,
a. IV fluids: This is administered in case of dehydration
- Loop diuretics (water pills): This is given to eliminate the excess fluid from the body, by facilitating frequent urination. This process of urination assists in the loss of sodium and potassium as well through the kidneys. Eg:- Furosemide (Lasix)
- Address the basic cause whenever possible. For instance, cease the gastrointestinal loss of fluid, correct hyperglycemia, control pyrexia, and withhold diuretics and lactulose. This is more than enough to revert the hypernatremic state.
- Where active hypernatremia correction needs to be undertaken, oral or enteral administration of fluids and IV therapy may be the last option.
- Hypernatremia management includes frequent observation of the patient’s condition and the sodium in blood, thereafter fixing the hypotonic infusion according to the sodium content.
Also, determine the following:-
Requirements of fluid
Deficiency of water:
The quantity of water that is required for returning the sodium in serum to a normal level can be evaluated by,
Water deficit = ((serum [sodium ion] (millimoles/liter)/145) – 1) x TBW
Here, L= water deficit, TWB = total water in the body that depends entirely on the amount of fat in the body; this varies according to age as well as sex. Thus, for calculating TBW, the lean weight of the body in kg is multiplied by,
- 0.6 – adult men and children
- 0.5 – elderly men and adult women
- 0.45- elderly women
But, in case of hypotonic fluid loss, where sodium loses along with free water, the total amount of water deficit is estimated to be greater than this amount.
Ongoing insensible loss of fluid:
This may prove to be helpful in certain cases for calculating the ongoing loss of free water through the urine resulting from the water clearance that is absolutely electrolyte-free or EFWC. It is calculated by,
EFWC = urine volume (1 – ((urinary [sodium ion] + urinary [potassium ion] +glucose in urine/2)/ serum [sodium ion]))
Here, the volume is expressed as L in concentrations of millimoles/litre.
Rate of correction
In chronic hypernatremia (> 24 hours/unknown duration), it is advisable to avoid correction of hypernatremia that is quicker than 0.5mmol/L/hour, and also at 10 to 12 millimoles/liter per day.
Initial free water replacement rate = water deficit x desired daily [Na+] reduction/desired total [Na+] reduction.
In such patients, it is recommended to decrease the sodium concentration in blood to somewhat near normal within a period of 24 hours to reduce the osmotic demyelination dangers and prevent the cerebral edema hazards.
Appropriate fluid amount
In case, significant hypovolaemia is seen, use 0.9 percent of saline isotonic fluid that is for restoring the circulating capacity.
In case, significant hypervolaemia is seen from hypertonic Na gain, then it is recommended to give diuretics along with 5% dextrose for offloading the fluid, and providing the deficient free water.
In times of simultaneous renal failure or if the sodium in blood > 170 mmol/L, it is recommended to consider filtration or hemodialysis. Or else, it is advisable to give hypotonic fluids, i. e., 0.45 % of saline, oral water, 5% of dextrose. However, it should be kept in mind that any Na or K-containing fluid is not equivalent to same free water proportion.
Monitoring the patient regularly, and conducting an electrolytes’ recheck throughout the alteration period, using hypotonic fluid and also modifying the rate or for maintaining the targeted correction rate.
- Subarachnoid hemorrhage
- Cerebral bleeding
- Permanent brain damage
- Death (this may be secondary to shrinking of brain with acute hypernatremia)
- Cerebral edema that corrects the chronic hypernatremia very fast.
- The prognosis in the treatment of hypernatremia is excellent, unless and until associated with neurological symptoms that are difficult to treat, and also reverses the condition.
- The rate of mortality mainly depends on the condition ‘severity and its onset speed.
- Mortality rate in severe hypernatremia is 40 to 70% as seen in the elderly patients. The consciousness level is the only excellent prognostic indicator related to mortality seen in the elderly population.
- A previous study conducted on the critically sick patients admitted in ICU, states that hypernatremia is an absolute risk factor in deciding mortality. In most cases, hypernatremia is seen after getting admitted to the ICU, and hence, may be partially iatrogenic.
- Take care of the hospitalized or chronically patients, as they are more prone to get hypernatremic.
- Pay attention to the fluid imbalance that may result due to hypernatremia.
- For preventing dehydration resulting from hypernatremia in infants on breast-feeding, lactation and early weighing is suggested, so that correctable problems can be identified early. For this, methods like rule of the thumb and daily weights are used in infants losing greater than 10 percentage of the total weight, especially in the postnatal 1st week. However, some feel that charts depicting ‘relative weight change’ are more beneficial screening strategies.