Management of Severe Hyponatremia and SIADH
Severe or acute hyponatremia carries high risk for cerebral edema, seizure and brain death, and requires intensive care unit (ICU) admission and urgent correction. A small immediate correction is sufficient for preventing these neurologic sequelae of hypo
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Robyn Scatena
Case Presentation A 51 year old woman with hypothyroidism, diabetes and hypertension presented with two weeks of progressive fatigue, weakness, and difficulty walking. In the emergency department she complained of lightheadedness and dizziness. Her initial blood pressure was 70/42. She was awake and alert, with 4/5 strength throughout. Her son had recently passed away and she reported decreased appetite, decreased oral intake, and weight loss. She had been smoking one pack of cigarettes per day since age 11. Initial serum sodium was 117 mmol/L, urine sodium 69 mmol/L, and urine osmolality 576 mOsm/kg. She was treated with 2 liters (L) of intravenous (IV) 0.9 % saline, and blood pressure improved to her baseline, 117/74. Question What is the cause of this patient’s severe hyponatremia, and with what urgency should it be corrected?
R. Scatena Yale University School of Medicine, New Haven, CT, USA Department of Medicine, Section of Pulmonary, Critical and Sleep, Norwalk Hospital, Norwalk, CT, USA e-mail: [email protected]
Answer Evaluate volume status and sodium balance, and correct slowly. Most patients with severe hyponatremia do not need urgent correction. Time should be taken to evaluate for underlying cause, treating slowly and monitoring sodium levels frequently. This patient was admitted with symptoms attributable to hyponatremia but no critical neurologic findings, so rapid sodium correction was not necessary. Initial IV fluids corrected blood pressure. At that point, the patient was euvolemic and still hyponatremic at 119 mmol/L. Urine sodium and osmolality were consistent with the syndrome of inappropriate antidiuretic hormone activity (SIADH), though measured serum osmolality results were not available. With SIADH the most likely diagnosis, fluids were restricted to 1 L per day and oral sodium chloride (NaCl) tablets begun. Serum sodium increased to 121 mmol/L by day 4 and the patient was transferred to the medical wards. Thereafter, she was found to be orthostatic and treated with IV normal saline. Serum sodium initially remained stable on IV fluids, and repeat studies demonstrated urine sodium 140 mmol/L, urine osmolality 389 mOsm/ kg, and serum osmolality 256 mOsm/kg, consistent with SIADH. By hospital day 10, despite resuming fluid restriction and escalating oral NaCl doses, serum sodium had decreased to 113 mmol/L, and the patient remained neurologically intact. Tolvaptan was begun and serum sodium increased to 120 mmol/L within 24 h, remaining stable in the mid-120s. Chest imaging
© Springer International Publishing Switzerland 2017 R.C. Hyzy (ed.), Evidence-Based Critical Care, DOI 10.1007/978-3-319-43341-7_46
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demonstrated a 2.5 cm left upper lobe nodule concerning for malignancy which proved to be the cause of her SIADH.
Principles of Management Risk Stratification
Table 46.1 Physical exam findings for volume status Hypovolemic Orthostasis Poor skin turgor Dry mucous membranes
Euvolemic Normal heart rate and blood pressure Normal ski
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