where Nae + and Ke + are total exchangeable quantities of these cations, and TBW is total body water. Therefore, hypernatremia can develop by a deficit in total body water and/or a gain of Na+.
Mechanisms of Hypernatremia
In a healthy individual, an increase in serum [Na+] and associated hyperosmolality create thirst, and water intake lowers serum [Na+] to a normal level (Chap. 11). Hypernatremia develops when patients:
1.
Cannot experience or respond to thirst
2.
Have no access to water
3.
Have salt loading
Patients at Risk for Hypernatremia
1.
Elderly
2.
Children
3.
Diabetics with uncontrolled glucose
4.
Patients with polyuria
5.
Hospitalized patients
Lack of adequate free water intake or administration
Impaired water conservation due to concentrating inability
Lactulose administration
Osmotic diuretics (mannitol)
Normal or hypertonic saline administration
Tube feedings or hyperalimentation
Mechanical ventilation
Approach to the Patient with Hypernatremia
Step 1: Estimate Volume Status
Based on volume status, classify hypernatremia into (Fig. 13.1):
Fig. 13.1
Classification and diagnostic approach to hypernatremia
1.
Hypovolemic hypernatremia (relatively more water than Na+ loss)
2.
Hypervolemic hypernatremia (relatively more Na+ than water gain)
3.
Normovolemic (euvolemic) hypernatremia (water loss with normal Na+)
Step 2: History and Physical Examination
History
Assess water intake and urine volume. Identify the cause of water loss. Is polyuria present? Polyuria is generally defined as urine volume > 3 L/day
Look for infusions of hypertonic saline, hyperalimentation or mannitol, including hyperglycemia for osmotic diuresis
Obtain history of diabetes, excessive sweating, or diarrhea that gives an idea of volume depletion
Take dietary history of high protein and electrolyte intake
Look for medications such as lactulose, loop diuretics, lithium, demeclocycline, and analgesics causing tubulointerstitial nephritis
Physical Examination
Vital signs and orthostatic changes (very important and mandatory). Record body weight
Examination of neck, lungs, heart for fluid overload, lower extremities for edema
Evaluation of mental status is extremely important
Step 3: Diagnosis of Hypernatremia
The most important tests besides urine volume are:
1.
Plasma and urine osmolalities
2.
Urine Na+ and K+
3.
Other laboratory tests such as serum K+, creatinine, BUN, Ca2+ are also helpful
4.
Brain imaging studies, as indicated
Electrolyte-free water clearance is useful during treatment of hypernatremia
Brain Adaptation to Hypernatremia
When serum [Na+] increases, the brain volume decreases due to exit of water and electrolytes, resulting in a decrease in intracranial pressure
However, within few hours, adaptive changes occur by moving water, electrolytes, and organic osmolytes (see Chap. 12) into the brain, and thereby returning brain volume to normal (Fig. 13.2).
Fig. 13.2
Adaptation of brain volume to hypernatremia
Signs and Symptoms of Hypernatremia
Mostly neurologic due to brain shrinkage and tearing of cerebral vessels
Acute hypernatremia: nausea, vomiting, lethargy, irritability, and weakness. These signs and symptoms may progress to seizures and coma
Chronic hypernatremia (present for > 1–2 days): less neurologic signs and symptoms because of brain adaptation; however, weakness, nystagmus, and depressed sensorium may be seen
Specific Causes of Hypernatremia
Polyuric syndromes constitute the most important causes of hypernatremia. These syndromes cause both water and solute (osmotic) diuresis. These patients usually have a urinary concentrating defect. Central DI, nephrogenic DI, and gestational DI cause water diuresis, whereas hyperalimentation, and infusions of hypertonic saline, glucose, and mannitol cause solute diuresis . Solute diuresis also occurs in patients with high BUN or during post-obstructive period. In these patients, polyuria causes polydipsia. Psychogenic polydipsia is considered under polyuric syndromes; however, it causes hyponatremia. In these patients, polydipsia causes polyuria. Figure 13.3 provides a simple approach to a patient with polyuria .
Fig. 13.3
Diagnostic approach to the patient with polyuria
Central DI
Central DI is due to failure to synthesize or release ADH from hypothalamus
Two types of central DI: complete and partial
Thirst mechanism is intact in most except in patients with craniopharyngiomas (post-operative)
Urine osmolality is usually ≤ 100 mOsm/kg H2O in complete form
Distal nephron responds to ADH action
Patients usually prefer ice or ice water, and nocturia is common
Causes are both congenital and acquired
Post-traumatic, post-surgical, metastatic tumors, granulomas, and CNS infections are the most common causes of acquired central DI
Treatment (see later text)
Nephrogenic DI
Nephrogenic DI is defined as tubular resistance to ADH action despite adequate circulating levels of ADH
Thirst mechanism is intact
Urine osmolality is < 300 mOsm/kg H2O
Causes are both congenital and acquired
Two forms of congenital nephrogenic DI have been described:
X-linked form (90 % of cases) due to loss-of-function mutation in vasopressin 2 receptor. Males with this mutation are characterized by dehydration, hypernatremia, and hyperthermia as early as the 1st week of life. Mental and physical retardation and renal failure are the consequences of late diagnosis
The second form has either autosomal dominant or recessive inheritance (10 % of cases). It is caused by loss-of-function mutation of AQP gene. Polyuria, dehydration, and hypernatremia are common. Carriers of AQP gene mutation are at risk for thromboembolism because of increased secretion of von Willebrand factor, the carrier protein for factor VIII
Treatment of both conditions includes hypotonic fluids to prevent dehydration. Hydrochlorothiazide alone or in combination with amiloride or indomethacin may be helpful in reducing urine output. Phosphodiesterase inhibitors, which prevent degradation of cAMP and cGMP, have been tried with variable success
Acquired nephrogenic DI: Important causes include CKD, hypokalemia, hypercalcemia, protein malnutrition, sickle cell disease, and lithium, or demeclocycline treatment. Table 13.1 describes the causes and mechanisms of acquired nephrogenic DI
Table 13.1
Some causes and mechanisms of acquired nephrogenic DI
Cause
Urine concentrating ability
cAMP generation
AQP2 expression
Management
CKD
Decreased
Decreased
Decreased
Match daily intake and output
Hypercalcemia
Decreased
Decreased
Decreased
Correct hypercalcemia
Hypokalemia
Decreased
Decreased
Decreased
Correct hypokalemia
Lithium
Decreased
Decreased
Decreased
Amiloride
Demeclocycline
Decreased
Decreased
Unknown
Discontinue the drug
Gestational DI
Occurs during late pregnancy and resolves after delivery
Caused by degradation of vasopressin (ADH) by the enzyme vasopressinase, and this enzyme is produced by the placenta
Treatment is desmopressin (dDAVP), which is not degraded by vasopressinase
Solute Diuresis
Occurs mostly in hospitalized patients except in those with uncontrolled hyperglycemia
Hospitalized patients develop solute diuresis because of infusion of normal or hypertonic saline, glucose, mannitol, or hyperalimentation
Note that glucose and mannitol initially cause hyponatremia; however, continued osmotic diuresis results in water deficit and hypernatremia
Urine osmolality is greater than plasma osmolality (> 300 mOsm/kg H2O), and urine osmoles (urine osmolality × urine volume) are > 900 mosmol/day
High BUN due to high protein intake can also cause solute diuresis and water deficit
Post-obstructive diuresis can also cause hypernatremia with sufficient water loss
Measurement of solute is the only way to recognize the cause of solute diuresis
Primary Hypodipsia
Refers to inadequate sensation of thirst with decreased water intake despite water availability
Subjects are usually elderly without hypothalamic or pituitary disease; however, these subjects have cerebrovascular accidents
Clinically they are hypovolemic with hypotension, dizziness, weakness, fatigue, confusion, and progression to seizures or coma
All patients have hypertonic urine without response to exogenous ADH
Hyperosmolality improves with hydration
Treatment is water 2–3 L
Essential Hypernatremia
A rare disorder with hypernatremia, hyperosmolality, and euvolemia
Patients are hypodypsic due to a pathologic lesion in hypothalamic-pituitary area
The threshold for ADH release and thirst is elevated
Fluid load fails to improve both hypernatremia and hyperosmolality
Both urinary dilution and concentrating ability are preserved
Essential hypernatremia is a counterpart of hyponatremia due to reset osmostat
Treatment is water 1–2 L/day
Diagnosis of Polyuria
The recommended test is water deprivation or dehydration test
Restrict fluid intake until urine osmolality reaches a plateau or until the patient loses 3–5 % of body weight. Avoid excess weight loss
Measure the highest serum and urine osmolalities
Administer 5 units of aqueous vasopressin subcutaneously
Measure urine osmolalities 30 and 60 min later
Compare the last urine osmolality before vasopressin and the highest urine osmolality after vasopressin, and note the difference between the two values
Table 13.2 provides the urine osmolality values after dehydration and following vasopressin in various polyuric conditions .
Table 13.2
Urine osmolalities (mmol/kg) in subjects with polyuric conditions in relation to normal subjects. (Data adapted from Miller et al. [1])
Subjects | Urine osmolality after dehydration | Urine osmolality increase after vasopressin (%) | Comment |
|---|---|---|---|
Normal | 1,000–1,137 | 0 to − 9 | Normal subjects do not respond to exogenous vasopressin, as these subjects have maximal release of vasopressin following dehydration |
Complete central DI
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