Treatment
Rapid correction of hyponatremia, even mild hyponatremia, risks neurologic complications
Generally, Na should be corrected no faster than 0.5 mEq/L/h. Increase
should not exceed 10 mEq/L over the first 24 h. Any identified cause of
hyponatremia is treated concurrently.
Mild hyponatremia:
Mild, asymptomatic hyponatremia (ie, plasma Na >
120 mEq/L) requires restraint. In diuretic-induced hyponatremia,
elimination of the diuretic may be enough; some patients need some Na
or K replacement. Similarly, if mild hyponatremia results from
inappropriate parenteral fluid administration in a patient with
impaired water excretion, merely stopping hypotonic fluid therapy may
suffice.
With hypovolemia, if adrenal function is normal,
administration of 0.9% saline usually corrects both hyponatremia and
hypovolemia. If the plasma Na is < 120 mEq/L, it may not completely correct upon restoration of intravascular volume; restriction of free water ingestion to ≤ 500 to 1000 mL/24 h may be needed.
In hypervolemic patients, in whom dilutional
hyponatremia is due to renal Na retention (eg, heart failure,
cirrhosis, nephrotic syndrome), water restriction combined with
treatment of the underlying disorder is often successful. An ACE
inhibitor, in conjunction with a loop diuretic, can correct refractory
hyponatremia in patients with heart failure. If hyponatremia does not
respond to simple fluid restriction, a loop diuretic in escalating
doses can be used, sometimes in conjunction with IV 0.9% normal saline.
K and other electrolytes lost in the urine must be replaced. If
hyponatremia is severe and unresponsive to diuretics, intermittent or
continuous hemofiltration may be needed to control ECF volume while
hyponatremia is corrected with IV 0.9% normal saline.
In euvolemia, treatment is directed at the cause (eg,
hypothyroidism, adrenal insufficiency, diuretic use). If SIADH is
present, severe water restriction (eg, 250 to 500 mL/24 h) is required.
Additionally, a loop diuretic may be combined with IV 0.9% saline as in
hypervolemic hyponatremia. Lasting correction depends on successful
treatment of the underlying disease. When the underlying disease is not
treatable, as in metastatic lung cancer, and severe water restriction
is unacceptable to the patient, demeclocycline (300 to 600 mg q 12 h)
may be helpful; however, demeclocycline may cause acute renal failure;
renal failure is usually reversible when the drug is stopped.
Investigational selective vasopressin receptor antagonists effectively produce water diuresis
without significant loss of electrolytes in the urine and may provide
useful future treatment for resistant hyponatremia.
Severe hyponatremia:
Severe hyponatremia (plasma Na < 109 mEq/L; effective osmolality <
238 mOsm/kg) in asymptomatic patients can be treated safely with
stringent restriction of water intake. Treatment is more controversial
when neurologic symptoms (eg, confusion, lethargy, seizures, coma) are
present. The debate primarily concerns the pace and degree of
hyponatremia correction. Many experts recommend that plasma Na be
raised no faster than 1 mEq/L/h, but replacement rates of up to 2
mEq/L/h for the first 2 to 3 h have been suggested for patients with
seizures. Regardless, the rise should be ≤ 10 mEq/L over the first 24 h. More vigorous correction risks precipitation of osmotic demyelination syndrome (see below).
Hypertonic (3%) saline (containing 513 mEq Na/L) may
be used, but only with frequent (q 2 to 4 h) electrolyte
determinations. For patients with seizures or coma, ≤
100 mL/h may be administered over 4 to 6 h in amounts sufficient to
raise the serum Na 4 to 6 mEq/L. This amount (in mEq) may be calculated
using the Na deficit formula as
(Desired change in Na) × TBW
where TBW is 0.6 × body weight in kg in men and 0.5 × body weight in kg in women.
For example, the amount of Na needed to raise the Na from 106 to 112 in a 70-kg man can be calculated as follows:
(112 mEq/L − 106 mEq/L) × (0.6 L/kg × 70 kg) = 252 mEq.
Because there is 513 mEq Na/L in hypertonic saline,
roughly 0.5 L of hypertonic saline is needed to raise the Na from 106
to 112 mEq/L. Adjustments may be needed, so plasma Na must be monitored
closely, beginning within the first 2 to 3 h after initiation of
treatment. Patients with seizures, coma, or altered mental status need
supportive treatment, which may involve airway intubation and
benzodiazepines (eg, lorazepam 1 to 2 mg IV q 5 to 10 min prn) for seizures.
Osmotic
demyelination syndrome:
Osmotic demyelination syndrome (previously called central pontine
myelinolysis) may follow too-rapid correction of hyponatremia.
Demyelination may affect the pons and other areas of the brain. Lesions
are more common in patients with alcoholism, malnutrition, or other
chronic debilitating illness. Flaccid paralysis, dysarthria, and
dysphagia can evolve over a few days or weeks. The lesion may extend
dorsally to involve sensory tracts and leave the patient with a
locked-in syndrome (an awake and sentient state in which the patient,
because of generalized motor paralysis, cannot communicate, except
possibly by coded eye movements). Damage often is permanent. If Na is
replaced too rapidly (eg, > 14 mEq/L/8
h) and neurologic symptoms start to develop, it is critical to prevent
further plasma Na increases by stopping hypertonic fluids. In such
cases, inducing hyponatremia with hypotonic fluid may mitigate the
development of permanent neurologic damage.
Bu yazıyı yazan Doktora ulaşım bilgileri:
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Prof. Dr. Yusuf AKCAN
Gastroenteroloji Uzm.
Ozel Istanbul Onkoloji Hastanesi
Tel. : 0 530 286 29 80
Tel. : 0 532 652 52 06
Cevizli Mah. Toros Cad. No : 86 PK:34846 Maltepe / Istanbul
( Gulsuyu Metro duragi karsisi)
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