Page 1376 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 99: Electrolyte Disorders in Critical Care 949

sodium has been raised by 4 to 6 mEq/L. Furthermore, the sodium
28
should be raised no more than 10- 12 mEq/L in the first 24 hours, and
by no more than 18 mEq/L in 48 hours. 30-34 The sodium concentration
should be assessed frequently to maintain the permitted rate of correction.
Aside from volume depletion, hypertonic saline is the best way to raise
the sodium concentration to treat acute, symptomatic hyponatremia.
When using hypertonic saline to correct hyponatremia, Eq. 99-4
allows rapid calculation of how much the serum sodium will change in
response to 1 L of IV fluid. It should be noted that when using IV fluids
to treat hyponatremia, potassium in the IV fluid has the same effect
on serum tonicity as sodium, and needs to be added to the sodium. 35,36
Figure 99-8 gives an example of using the change in sodium formula to
manage hyponatremia.
Caution should be used when estimating total body water. The
common estimate of 0.7 times total body weight for men and 0.6 times
total body weight for women assumes a normal hydration status and
normal percentage of body fat. This calculation overestimates total body
water among patients who are volume depleted or obese. Overestimating
TBW leads to exceeding limits on the speed of correction and possibly
increased risk of osmotic demyelination.
FIGURE 99-7. Decreases in extracellular osmolality cause the intracellular compartment In the setting of hyponatremia due to volume depletion, normal saline
to be relatively hypertonic. The hypertonic intracellular compartment attracts water, result- should be used to restore normal perfusion prior to specific therapy for
ing in cellular swelling and tissue dysfunction. In the brain, cellular swelling causes cerebral hypoosmolality. Restoring normal perfusion will remove the nonos-
edema and elevated intracranial pressure. motic stimulus for ADH release so the kidney will increase free water
clearance and autocorrect the hyponatremia. In some situations, patients
will correct their sodium too fast and require free water infusions to slow
the rate of correction.
intracellular solutes, lowering intracellular volume. With the restora-
tion of intracellular volume in chronic hyponatremia, the condition Asymptomatic Hyponatremia Whereas acute symptomatic hyponatremia
becomes essentially asymptomatic. demands aggressive treatment to reverse cerebral edema, chronic
Hypoxia is repeatedly reported as a common finding among patients asymptomatic hyponatremia is well tolerated and should be treated
with symptomatic hyponatremia. Some authors have attributed this to conservatively. First, any ongoing cause of the hyponatremia (eg, water
noncardiogenic pulmonary edema, though central hypoventilation may intake or diuretics) should be stopped and water restriction initiated.
28 ) A spot urine sodium and potassium should be checked in order to
also be responsible. The average partial arterial oxygen pressure (Pa O 2
of patients with symptomatic hyponatremia was 63 mm Hg and 68% of calculate the C EFW . In most cases, this will be positive and can allow one
the patients in this series were ultimately intubated. Hypoxia has been to determine the degree of fluid restriction required to raise the serum
29
shown to delay cellular compensation, resulting in persistent symptoms sodium. However, in SIADH the C EFW will be negative, which means
of acute hyponatremia despite a prolonged clinical course of over 5 days. that for every milliliter of urine the patient produces, water is added to
(rather than cleared from) the body. With a negative C water restric-
EFW
Treatment: Hyponatremia causes symptoms due to cerebral edema tion will rarely be successful at raising serum sodium. In this unique
from the osmotic movement of water into cells. Compensation for situation, a loop diuretic can increase the C by reducing the urine
EFW
acute hyponatremia consists of cells ejecting intracellular solutes in sodium. A negative C only occurs when the urine Na plus urine K is
EFW
order to restore normal cell volume. This compensation complicates higher than the serum Na, and loop diuretics typically reduce the urine
treatment decisions because rapidly restoring normal osmolality in sodium to around 70, which is sufficient to reduce the urine Na plus K
the presence of compensated cells can cause the serum to be relatively to below serum Na. This will make the C positive and allow fluid
hypertonic to the cells, resulting in the osmotic movement of water EFW
out of the cells. In the CNS, this can cause a condition called central
pontine myelinolysis (CPM) or osmotic demyelination syndrome
(ODS) that results in severe morbidity or death. In determining
the treatment plan for hyponatremia, one must balance the risk of Initial Na = 107 mmol/L
cerebral edema from the hyponatremia against the risk of ODS from
treating compensated hyponatremia. Creating evidence-based guide- Na = V iv × (Na + K ) − V × (Na + K ) − V × Na s
u
iv
iv
u
u
lines is difficult because of the lack of randomized controlled trials. TBW + V
Recommendations are based on retrospective case series and expert 1 × (513 + 40) − 1 × 107
opinion. The following guidelines attempt to balance the risks of these Na = 42 + 1
opposing outcomes.
Symptomatic Hyponatremia In acute hyponatremia, little compensation has Na = 10.4
occurred and the benefits of rapid correction and resolution of cerebral So : 1 L of 3% saline will increase Na by 10 and 1.2 L will increase it by 12,
edema outweigh the risks of ODS. While acute hyponatremia has clas- the limit for the first day of therapy.
sically been defined as hyponatremia lasting less than 48 hours, a pro- To calculate the rate, divide 1200 mL by 24 hour:
spective (albeit not randomized) trial has shown active treatment to be 1200 mL
superior to fluid restriction for a cohort of patients with CNS symptoms 24 h = 50 mL/h
and an average duration of hyponatremia of 5.2 days (all had hypona-
tremia for longer than 48 hours and a gradual decrease in sodium of FIGURE 99-8. Using the change in sodium formula to assist with the treatment of hypo-
0.5 mmol/L per hour). Given this, patients with symptomatic hypona- natremia. In this example, the patient is assumed to be anuric. During the treatment urine Na
tremia regardless of duration should be actively treated. Sodium levels and K should be measured along with urine volume to better refine the estimated volume and
should be initially raised rapidly until symptoms abate or the serum time needed to correct the hyponatremia.

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