Chapter 046. Sodium and Water (Part 7) potx

Chapter 046. Sodium and Water
(Part 7)

Diagnosis
(Fig. 46-1) Hyponatremia is not a disease but a manifestation of a variety of
disorders. The underlying cause can often be ascertained from an accurate history
and physical examination, including an assessment of ECF volume status and
effective circulating arterial volume. The differential diagnosis of hyponatremia,
an expanded ECF volume, and decreased effective circulating volume includes
congestive heart failure, hepatic cirrhosis, and the nephrotic syndrome.
Hypothyroidism and adrenal insufficiency tend to present with a near-normal ECF
volume and decreased effective circulating arterial volume. All of these diseases
have characteristic signs and symptoms. Patients with SIADH are usually
euvolemic.
Figure 46-1

Algorithm depicting clinical approach to hyponatremia. ECF,
extracellular fluid; SIADH, syndrome of inappropriate antidiuretic hormone
secretion.
Four laboratory findings often provide useful information and can narrow
the differential diagnosis of hyponatremia: (1) the plasma osmolality, (2) the urine
osmolality, (3) the urine Na
+
concentration, and (4) the urine K
+
concentration.
Since ECF tonicity is determined primarily by the Na
+
concentration, most
patients with hyponatremia have a decreased plasma osmolality. The appropriate
renal response to hypoosmolality is to excrete the maximum volume of dilute

urine, i.e., urine osmolality and specific gravity of <100 mosmol/kg and 1.003,
respectively. This occurs in patients with primary polydipsia. If this is not present,
it suggests impaired free-water excretion due to the action of AVP on the kidney.
The secretion of AVP may be a physiologic response to hemodynamic stimuli or it
may be inappropriate in the presence of hyponatremia and euvolemia. Since Na
+
is
the major ECF cation and is largely restricted to this compartment, ECF volume
contraction represents a deficit in total body Na
+
content. Therefore, volume
depletion in patients with normal underlying renal function results in enhanced
tubule Na
+
reabsorption and a urine Na
+
concentration <20 mmol/L. The finding
of a urine Na
+
concentration >20 mmol/L in hypovolemic hyponatremia implies a
salt-wasting nephropathy, diuretic therapy, hypoaldosteronism, or occasionally
vomiting. Both the urine osmolality and the urine Na
+
concentration can be
followed serially when assessing response to therapy.
SIADH is characterized by hypoosmotic hyponatremia in the setting of an
inappropriately concentrated urine (urine osmolality >100 mosmol/kg). Patients
are typically normovolemic and have normal Na
+
balance. They tend to be mildly

volume-expanded secondary to water retention and have a urine Na
+
excretion rate
equal to intake (urine Na
+
concentration usually >40 mmol/L). By definition, they
have normal renal, adrenal, and thyroid function and usually have normal K
+
and
acid-base balance. SIADH is often associated with hypouricemia due to the
uricosuric state induced by volume expansion. In contrast, hypovolemic patients
tend to be hyperuricemic secondary to increased proximal urate reabsorption.
Hyponatremia: Treatment
The goals of therapy are twofold: (1) to raise the plasma Na
+
concentration
by restricting water intake and promoting water loss and (2) to correct the
underlying disorder. Mild asymptomatic hyponatremia is generally of little clinical
significance and requires no treatment. The management of asymptomatic
hyponatremia associated with ECF volume contraction should include Na
+

repletion, generally in the form of isotonic saline. The direct effect of the
administered NaCl on the plasma Na
+
concentration is trivial. However,
restoration of euvolemia removes the hemodynamic stimulus for AVP release,
allowing the excess free water to be excreted. The hyponatremia associated with
edematous states tends to reflect the severity of the underlying disease and is
usually asymptomatic. These patients have increased total body water that exceeds

the increase in total body Na
+
content. Treatment should include restriction of Na
+

and water intake, correction of hypokalemia, and promotion of water loss in
excess of Na
+
. The latter may require the use of loop diuretics with replacement of
a proportion of the urinary Na
+
loss to ensure net free-water excretion. Dietary
water restriction should be less than the urine output. Correction of the K
+
deficit
may raise the plasma Na
+
concentration by favoring a shift of Na
+
out of cells as
K
+
moves in. Water restriction is also a component of the therapeutic approach to
hyponatremia associated with primary polydipsia, renal failure, and SIADH
(Chap. 334). The recent development of nonpeptide vasopressin antagonists has
introduced a new selective treatment for euvolemic and hypervolemic
hyponatremia.