Page 1374 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 99: Electrolyte Disorders in Critical Care 947

with pseudohyponatremia have normal sodium and osmolality, no
Initial Na = 168 mmol/L
specific treatment is needed.
With simultaneous hyponatremia and hyperosmolality, an additional
V × (Na + K ) − V × Na
Na = iv iv iv s solute is contributing to the osmolality. Both glucose and mannitol
TBW + V
can act as the additional solute. The increased extracellular osmolality
Na = 1 × (0 + 0) − 1 × 168 draws water from the intracellular space, diluting serum sodium. The
42 + 1 measured serum sodium falls by a predictable amount; the common
cited adjustment is a decrease in sodium of 1.6 mmol/L for every
Na = 3.9 4 100 mg/dL increase in blood glucose. However, the only empiric data
12
So: 6 L free water will decrease Na by 24 to 144 mmol/L that looked at this showed a more complex relationship: The adjustment
To calculate the rate, limited to 2 mmol/L per hour: of 1.6 mmol/L holds until serum glucose exceeds 400 mg/dL, at which
point the sodium should fall by 4.0 mmol/L for every 100 mg/dL rise
24 mmol/L × 6 L = 0.5 L/h in glucose. For glucose less than 700 mg/dL, using an adjustment of
2 mmol/L per hour
2.4 worked nearly as well as the more complex biphasic system. 13
Hyposmotic hyponatremia, also called true hyponatremia, and in
FIGURE 99-4. Using the change in sodium formula to assist with the treatment of hyper- the remainder of the chapter simply called hyponatremia, occurs when
natremia. In this example the patient is assumed to be anuric. During the treatment urine Na electrolyte-free water intake exceeds electrolyte-free water clearance
and K should be measured along with urine volume to better refine the estimated volume and (C ). Intact kidneys are able to clear close to 20 L of electrolyte-free
EFW
time needed to correct the hypernatremia. See caption to Eq. 99-4 for explanation of variables. water, so outside of exceptional water intake, hyponatremia only occurs
when there is a defect in the C EFW . This defect in C EFW can alternatively
be stated as an inability to produce an adequate volume of dilute urine.
serum sodium from a given amount of fluid can be calculated using This can be due to
Eq. 99-4. An example of this is shown in Figure 99-4.
A number of complications from the treatment of hypernatremia • Decreased delivery of water to the diluting segments of the nephron,
can occur. If the sodium is lowered too quickly, cerebral edema may namely the thick ascending limb of the loop of Henle (TALH) and
occur. Dextrose solutions predispose patients to hyperglycemia, which distal convoluted tubule (DCT). Decreased delivery of tubular fluid
may cause an osmotic diuresis, worsening the hypernatremia. For this is due to a generalized decrease in glomerular filtration rate (GFR),
reason, enteral fluids are preferred during treatment of hypernatremia. as seen in renal failure, or increased proximal resorption of water, as
■ HYPONATREMIA • Decreased activity in the diluting segments of the nephron due to
seen with decreased EABV.
Hyponatremia is defined as a serum sodium less than 136 mmol/L. Since diuretics. Loop diuretics block solute resorption in the TALH and
serum sodium and its accompanying anions are the principal determi- thiazide-type diuretics block resorption in the DCT.
nants of serum osmolality, hyponatremic patients are typically hypoos- • ADH activity, which allows water to be resorbed in the collecting
molar; however, hyponatremia may also be associated with normal or tubules, preventing C EFW .
elevated osmolality. Since the primary morbidity from hyponatremia is
due to decreased tonicity, hyponatremia with normal or elevated osmo- Etiologies: Hypotonic hyponatremia is traditionally broken down by
clinical volume status of the patient (Table 99-3). While this may help
lality does not cause the clinical picture typically associated with the
more typical hyponatremia with decreased tonicity. clinically classify patients, it does not elucidate the pathophysiology
of hyponatremia (eg, CHF and vomiting both cause hyponatremia by
Pseudohyponatremia is associated with a normal plasma osmolality.
It is an artifact of two popular sodium assays, flame photometry and inducing a nonosmotic release of ADH, but they are on opposite sides
of the classification, as one is hypovolemic and the other hypervol-
indirect potentiometry. Serum with elevated triglycerides, proteins
(from multiple myeloma or Waldenström macroglobulinemia, or fol- emic). A pathophysiologic approach to hyponatremia categorizes the
.
etiology based on why the patient has compromised C
lowing intravenous immunoglobulin therapy), or rarely cholesterol EFW
has increased solute, and thus a given volume of serum contains less Decreased Delivery of Water to the Diluting Segments of the Nephron Decreases in GFR
water. This results in a lab error due to overdilution of the sample for any reason reduce C EFW . Patients with renal failure must moderate
(Fig. 99-5). Patients suspected of having pseudohyponatremia should their intake of fluids or they may develop acute hyponatremia. Decreases
have their sodium assessed by direct potentiometry, a technique gener- in effective arterial blood volume can result from heart failure, cirrhosis,
ally employed by blood gas laboratories that is not susceptible to arti- or volume depletion. Even in situations in which the GFR is intact,
factual hyponatremia. Indirect potentiometry is used in two-thirds of decreased EABV (due to CHF, liver failure, or nephrotic syndrome)
clinical labs, making pseudohyponatremia a real issue. Since patients increases resorption of fluid in the proximal tubule, reducing delivery
11
of fluid to the diluting segments. Patients with reduced distal delivery
of fluid have positive C EFW , but the clearance is less than their intake of
free water. The hyponatremia tends to be gradual in onset and of mild
Normal Pseudohyponatremia
severity.
Decreased Activity in the Diluting Segments of the Nephron Due to Diuretics An intact
diluting segment is essential to C . In some patients, severe hypona-
Protein, lipid EFW
tremia can follow the initiation of diuretics. Diuretics promote hypo-
14
Plasma Plasma natremia by blocking at least one and possibly all three factors required
Plasma water
to produce dilute urine:
1. Thiazide and loop diuretics both directly antagonize the production
RBC of dilute urine.
2. Diuretic-induced volume depletion reduces the delivery of water to
FIGURE 99-5. Pseudohyponatremia occurs when plasma proteins or lipids occupy an the diluting segments of the nephron.
unexpectedly high volume. The decreased plasma water is overdiluted while preparing the 3. With more dramatic volume loss, diuretics stimulate a nonosmotic
sodium assay, so the sodium will be falsely reported as low. release of ADH, dramatically reducing C
EFW.

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