TRIPASS XR تري باس

 

15

Most patients who are edematous and hyponatremic are asymptomatic, but the

degree of hyponatremia probably reflects the severity of the underlying disease.

46,47,49

Unless an acute decrease in serum sodium occurs, rapid therapeutic correction is not

warranted.

37,40,46,47,50 Water restriction, the mainstay of therapy, is determined by the

degree of hyponatremia and the severity of symptoms. Sodium restriction and

judicious use of diuretics may help reduce the edematous state, but the patient must

be monitored closely to avoid prerenal azotemia, which suggests overaggressive

diuresis. Furthermore, diuretics can induce or worsen hyponatremia and volume

depletion by impairing the diluting capacity of the kidney.

43–47

T.W. had abdominal paracentesis to relieve respiratory discomfort with no

sequelae. He was then prescribed a 1,000-mg sodium diet, and water was restricted

to 500 mL/day. Diuretic therapy was resumed.

Normovolemic Hypotonic Hyponatremia

CASE 27-7

QUESTION 1: C.C., a 50-year-old man who was diagnosed recently with small-cell lung carcinoma, was

brought to the ED by his family because he had become progressively lethargic and stuporous during the past

week. Laboratory data revealed the following:

Serum Na, 110 mEq/L

K, 3.6 mEq/L

Cl, 78 mEq/L

Bicarbonate, 22 mEq/L

BUN, 10 mg/dL

SCr, 0.9 mg/dL

Glucose, 90 mg/dL

Serum osmolality, 230 mOsm/kg

Urine osmolality, 616 mOsm/kg

Urine Na, 60 mEq/L

Arterial blood gas (ABG) examination at room air showed pH, 7.38; PCO2

, 38 mm Hg; and PO2

, 80 mm

Hg. On physical examination, C.C. was normotensive, appeared to be euvolemic, and had no edema detected.

Review of his medical records showed normal adrenal and thyroid function. C.C. was currently not using any

medications. On admission to the ward, C.C. weighed 60 kg and was given 1 L of normalsaline, after which his

serum sodium concentration was 108 mEq/L. Identify the cause of hyponatremia in C.C. and describe its

pathophysiology.

In a patient with hypo-osmolar hyponatremia with a volume status that is

apparently normal, the differential diagnosis

40

includes hypothyroidism,

51 cortisol

deficiency,

52 a reset osmostat,

53 psychogenic polydipsia,

36,38 and the syndrome of

inappropriate antidiuretic hormone secretion (SIADH),

54–56 which is a diagnosis of

exclusion. C.C.’s normal thyroid and adrenal function tests exclude hypothyroidism

and cortisol insufficiency as causes of his hyponatremia. The inappropriately

elevated urine osmolality (>100 mOsm/kg) is inconsistent with psychogenic

polydipsia or a reset osmostat, because free-water excretion is usually not impaired

in these disorders. These findings, in addition to a urine sodium concentration greater

than 40 mEq/L and a normal acid–base and potassium balance, are consistent with

SIADH.

37,55,56

In SIADH, the ADH secretion is considered inappropriate because of its

persistence in the absence of appropriate osmotic and hemodynamic stimuli. Water

ingestion is essential to the development of hyponatremia in SIADH because

persistent ADH activity impairs water excretion, resulting in expansion of body

fluids and hypo-osmolar hyponatremia. Edema rarely is apparent because only onethird of the retained water resides in the extracellular space and the sodium

homeostatic mechanisms are intact.

34,40 The ECF expansion activates volume

receptors and results in natriuresis. At steady state, urinary sodium excretion reflects

sodium intake and is usually greater than 40 mEq/L, as in C.C.’s case. Nonetheless, if

sodium intake is reduced severely, the urinary sodium concentration may become less

than 40 mEq/L.