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Stroke vs. SIADH: A case of symptomatic hyponatremia secondary to SIADH in association with COVID-19 infection

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A 66-year-old male with no known past medical history presented with history of two days of throbbing frontal headache associated with nausea, vomiting and left-sided facial droop. The patient also reported dizziness, subjective chills without cough, shortness of breath, or sputum production. Laboratory findings revealed elevated inflammatory markers but normal thyroid, kidney, and liver function tests. Initial sodium level was 126 mEq/L. Urine studies showed elevated urine osmolality of 647 mOsm/Kg and urine sodium level of 175 mEq/L, both suggestive of syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The TSH and ACTH stimulation tests both came back as normal. CT scan of the chest showed no evidence of lung infiltrates. Diffusion weighted MRI of the brain showed no evidence of acute or subacute CVA. SARS-CoV-2 nasal swab test was resulted positive. With these findings we diagnosed our patient with SIADH. Patient was initially started on 3% saline infusion for symptomatic hyponatremia. A fluid restricted diet was enforced. Patient was also started on salt tablets in order to increase solute intake. Sodium slowly corrected throughout the hospitalization. Of note, our patient never became hypoxic, neither did he show evidence of clinical pneumonia. A CT imaging of the chest showed no lung infiltrates, and an MRI of the brain was negative for any acute intracranial abnormalities. This case highlights the role of early recognition of SIADH in the setting of SARS-CoV-2 infection even in the absence of hypoxemia or lung pathology.
Title: Stroke vs. SIADH: A case of symptomatic hyponatremia secondary to SIADH in association with COVID-19 infection
Description:
A 66-year-old male with no known past medical history presented with history of two days of throbbing frontal headache associated with nausea, vomiting and left-sided facial droop.
The patient also reported dizziness, subjective chills without cough, shortness of breath, or sputum production.
Laboratory findings revealed elevated inflammatory markers but normal thyroid, kidney, and liver function tests.
Initial sodium level was 126 mEq/L.
Urine studies showed elevated urine osmolality of 647 mOsm/Kg and urine sodium level of 175 mEq/L, both suggestive of syndrome of inappropriate secretion of antidiuretic hormone (SIADH).
The TSH and ACTH stimulation tests both came back as normal.
CT scan of the chest showed no evidence of lung infiltrates.
Diffusion weighted MRI of the brain showed no evidence of acute or subacute CVA.
SARS-CoV-2 nasal swab test was resulted positive.
With these findings we diagnosed our patient with SIADH.
Patient was initially started on 3% saline infusion for symptomatic hyponatremia.
A fluid restricted diet was enforced.
Patient was also started on salt tablets in order to increase solute intake.
Sodium slowly corrected throughout the hospitalization.
Of note, our patient never became hypoxic, neither did he show evidence of clinical pneumonia.
A CT imaging of the chest showed no lung infiltrates, and an MRI of the brain was negative for any acute intracranial abnormalities.
This case highlights the role of early recognition of SIADH in the setting of SARS-CoV-2 infection even in the absence of hypoxemia or lung pathology.

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