Appeal type: Medical necessity
Decision: Overturned

Diagnosis:  Hyponatremia.
Treatment:  Inpatient Admission.

The insurer denied coverage for inpatient admission.  The denial is overturned.

The patient is an elderly female who presented with hyponatremia. She was noted to have nausea, abdominal pain and diarrhea. She stated that she was having diarrhea for two days. On presentation she was noted to be afebrile and hemodynamically stable. On physical examination her abdomen was noted to be unremarkable. Her initial sodium level was 123 mmol/L (millimoles per liter). It was thought that her hyponatremia was secondary to dehydration. The patient was made nothing per mouth and given a fluid bolus of normal saline. She was then started on normal saline at a rate of 50cc (cubic centimeters) per hour. It was thought that her hyponatremia was secondary to her Hydrochlorothiazide (HCTZ) and diarrhea.

The patient needed to be admitted to receive sodium replacement since her sodium level was noted to be dangerously low. The patient also needed to be monitored to evaluate for neurological complications that can occur with overcorrection of sodium. 

Filippone, E. J., Ruzieh, M., & Foy, A. (2020), "Hyponatremia can complicate thiazide use in a minority of susceptible individuals and can result in significant morbidity and even mortality. Risk factors for thiazide-associated hyponatremia include age, female sex, and possibly low body mass. A genetic susceptibility has recently been uncovered. Although frequently developing early after thiazide treatment initiation, many cases of hyponatremia present after months or years of use. Many cases are asymptomatic or have mild symptoms, but seizures and/or coma may develop, especially in those with acute onset. The pathophysiology is incompletely understood and includes some combination of excessive fluid intake, cation (sodium and potassium) depletion, osmotic inactivation of sodium, and reduced ability to excrete free water. Reduced distal delivery of filtrate, reduced solute load (urea), direct inhibition of the sodium-chloride cotransporter, and increased collecting duct permeability to water mediated by some combination of antidiuretic hormone, prostaglandins, and thiazides themselves may contribute to this diluting defect. The predominant pathophysiologic mechanism(s) varies from patient to patient. The cornerstone of therapy is cessation of thiazide use, cation repletion, and oral fluid restriction. If severely symptomatic, 3% saline solution may be indicated. Overly rapid correction of chronic hyponatremia must be avoided in all cases."

Burst, V., Grundmann, F., Kubacki, T., Greenberg, A., Becker, I., Rudolf, D., & Verbalis, J. (2017), "Thiazide was withdrawn immediately after hyponatremia was diagnosed only in 57% of TAH; in these patients, the median rate of [Na+] change (daily[Na+]) was significantly higher than those with continued thiazide treatment (3.8 [interquartile range: 4.0] vs. 1.7 [3.8] mEq/L/day). The most frequently employed therapies were isotonic saline (29.6%), fluid restriction (19.9%), the combination of these two (8.2%), and hypertonic saline (5.2%). Hypertonic saline produced the greatest daily [Na+] (8.0[6.4] mEq/L/day) followed by a combination of fluid restriction and normal saline (4.5 [3.8] mEq/L/day) and normal saline alone (3.6 [3.5] mEq/L/day). Fluid restriction was markedly less effective (2.7 [2.7] mEq/L/day). Overly rapid correction of hyponatremia occurred in 3.1% overall, but in up to 21.4% given hypertonic saline. Although there are highly significant differences in the biochemical profiles between TIH and SIADH, no predictive diagnostic test could be derived."

Based on the above, the insurer's denial must be overturned. The health care plan did not act reasonably and with sound medical judgment and in the best interest of the patient. The medical necessity for inpatient admission is substantiated.