A Rare Cause of Worsening Hyponatremia in Pulmonary SIADH
- Fluid, Electrolyte, Acid-Base Disorders: Clinical - II
November 04, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
- Bector, Shorya, Icahn School of Medicine at Mount Sinai, New York, New York, United States
- Bector, Yachit, Baba Farid University of Health Sciences, Faridkot, Punjab, India
Primary adrenal insufficiency is a relatively rare entity with most cases in the United States secondary to auto-immune or genetic processes. Here we present a rare case of tuberculous adrenalitis presenting as worsening hyponatremia in a patient with SIADH.
50-year-old male from Mexico, with medical history of pulmonary tuberculosis and chronic hyponatremia (SIADH secondary to tuberculosis), presented with complaints of generalized weakness, nausea and vomiting for 4 days. Initial lab evaluation was significant for hyponatremia of 119. This was a significant change from patient’s previous mild hyponatremia readings in 130s which had responded to salt tablets and fluid restriction in the past. This led to further investigation into the cause of this worsening hyponatremia not responsive now to salt tablets or fluid restriction. Labs were significant for low cortisol with no increase seen with ACTH stimulation test, suggestive of primary adrenal insufficiency, subsequently confirmed by high ACTH. Imaging revealed interval worsening of pulmonary tuberculosis with left upper lobe opacity, scattered patchy opacities and tree-in-bud nodularity in lingula, left lower lobe and right upper lobes. Bilateral adrenal hyperplasia and retroperitoneal adenopathy were noted on abdominal CT scan. Patient was re-started on RIPE therapy and hydrocortisone and fludrocortisone supplementation requiring higher doses due to RIPE. Patient’s symptoms improved and sodium stabilized in 130s after therapy initiation.
Adrenal insufficiency generally appears in tuberculosis cases after 90% glandular destruction. Most patients with active disease have bilateral adrenal enlargement seen on imaging and biopsy is generally not required in cases with evidence of extra-adrenal tuberculosis. This case was unique as there was clear evolution in the cause of hyponatremia with worsening infection. It also highlighted the importance of investigating worsening of chronic hyponatremia in patients with pulmonary tuberculosis. Lastly, it should be highlighted that even with treatment of the infection, adrenal function rarely seems to return to normal likely due to anatomical destruction of the gland, emphazing the importance of early detection and medication compliance in this disease.