Hyponatremia Case Study

A 72-year-old male presents to his physician, complaining that he is coughing blood-tinged sputum. The patient states that he has been a heavy smoker all of his life and has coughed up yellow sputum every morning for years now, but the sputum has never had blood in it before. On review of systems, the patient says that he has been feeling tired recently and has lost 5.4 kg (12 lb) despite no change in his diet.

Vital signs: Temp 37.2ºF (99°F), blood pressure 110/76 mmHg, heart rate 88 beats/min, respiratory rate 14 breaths/min.

Physical examination is unremarkable with no evidence of leg edema, lung crepitations, heart S3 sound, or ascites. Skin turgor is normal. Laboratory studies show a normal urinalysis and CBC, with comprehensive chemistry

panel seen in the image. A chest x-ray is seen in the image. The next best step in patient management is:
Comprehensive Metabolic Panel

Patient Reference range
Sodium 124 136–145 mEq/L
Potassium 3.9 3.5–5.1 mEq/L
Bicarbonate 27 23–29 mEq/L
Chloride 101 98–107 mEq/L
Glucose 84 70–99 mg/dL
Creatinine 0.9 0.6–1.1 mg/dL
BUN 4.2 6–20 mg/dL
Calcium 9.8 8.6–10.2 mg/dL
Total protein 6.6 6–7.8 mg/dL
Albumin 4.3 3.5–5.5 mg/dL
Total bilirubin 1 0.1–1.1 mg/dL
ALT 32 10–40 U/L
AST 31 10–40 U/L
Alkaline phosphatase 65 20-70 U/L

A. Conivaptan
B. Fluid restriction
C. Hypertonic saline
D. Isotonic saline
E. Thiazide diuretic

Answer

Choice "B" is the best answer. The patient presents with a central lung mass as an obvious cause of his hemoptysis. The history of heavy cigarette smoking, location of the tumor, and symptoms all make invasive carcinoma the most likely pathology. This would require tissue confirmation, most likely by fine needle aspirate (FNA) if the staging CT scan did not show lymph node involvement. Central carcinomas of lung are usually squamous cell carcinomas or small cell carcinomas, as compared to adenocarcinomas, which are peripheral in location and not closely linked to smoking.
The chemistry panel shows a mild hyponatremia. The usual investigative approach to hyponatremia first starts with an evaluation of the patient’s volume status, as seen in the algorithm. This patient has no history of vomiting or diarrhea and no evidence of congestive heart failure (clear lung fields and no S3), renal failure (normal creatinine), or ascites (normal liver values and negative physical examination). There is no increase in serum glucose to suggest an osmotic diuresis, nor proteinuria to suggest nephrotic syndrome. This makes serum inappropriate ADH (SIADH) secretion the most likely cause. If there was any doubt in this diagnosis, serum osmolarity (normal to low) could be compared to urine osmolarity (high). The source of ADH in this patient is probably the lung carcinoma. This will be established by the biopsy showing a small cell carcinoma.

Hyponatremia, defined as a serum sodium level < 135 mEq/mL, is classified as mild (serum sodium > 120 mEq/mL) or severe (serum sodium < 110–115 mEq/mL), and acute (hours to days) or chronic (weeks to months).

Symptoms are not usually present in mild chronic hyponatremia, as is seen with this patient. Symptoms are more likely when there is a rapid decrease in serum sodium levels and when sodium is < 120 mEq/mL. In asymptomatic SIADH, fluid restriction will restore the serum sodium to normal. Treatment of the small cell carcinoma with chemotherapy should give a permanent end to the source of the ADH. Restriction to 50% to 60% of daily fluid requirements may be required to achieve the goal of inducing negative water balance. In general, fluid intake should be less than 800

mL/day.

Choice "A" is not the best answer.

The vasopressin receptor antagonists may provide an alternative treatment for SIADH. They produce a selective water diuresis without affecting sodium and potassium excretion. Conivaptan specifically blocks the V2 receptor. The ensuing loss of free water tends to correct the hyponatremia. However, thirst increases significantly with these agents, which may limit the rise in serum sodium. Also, they may cause too rapid a rise in sodium levels, they are expensive, and there may be adverse effects. Water restriction is a safe and simple first choice.

Choice "C" is not the best answer. More aggressive therapy is indicated in patients who have symptomatic or severe hyponatremia. In this setting, initial therapy usually consists of hypertonic saline with or without vasopressin receptor antagonists. The rate of correction is important because too-rapid correction of severe hyponatremia can lead to osmotic demyelination (aka central pontine demyelinosis). One group that is probably not at risk for this complication is patients with hyperacute hyponatremia that develops over a few hours due to a marked increase in water intake, as may be seen in marathon runners, psychotic patients, and users of 3,4-methylenedioxy-methamphetamine (MDMA;

Ecstasy).
Choice "D" is not the best answer. Sodium chloride, usually as isotonic saline or increased dietary salt, is given to patients with true volume depletion and/or adrenal insufficiency. Salt therapy is generally contraindicated in edematous patients (e.g., heart failure, cirrhosis, renal failure) because it will lead to exacerbation of the edema.
Choice "E" is not the best answer. Using a thiazide to block the distal convoluted tubule’s Na-Cl symporter will not correct the problem. Use of a loop diuretic may be beneficial in patients with SIADH because, by inhibiting sodium chloride reabsorption in the thick ascending limb of the loop of Henle, it interferes with the countercurrent mechanism and induces a state of ADH resistance, and a more dilute urine is excreted.