Posters
Presentation Type
Poster
Discipline Track
Patient Care
Abstract Type
Case Report
Abstract
Background: Subclinical hypothyroidism is biochemically defined with normal serum-free T4 in the presence of an elevated serum TSH. Common symptoms of an underactive thyroid can include fatigue, weakness, cold intolerance, weight gain despite poor appetite, hair loss, constipation, and depression. Pleural effusions have also been recognized as a clinical sequelae in the literature, where up to 25% of patients can develop a pleural fluid collection in the setting of hypothyroidism. Although not well understood, a mechanism includes an increased capillary permeability that leads to the retention of fluid in pleural cavities and other tissues.
Case presenting: A 66-year-old woman with PMH of hypertension and Type 2 DM presented to the hospital complaining of acute progressive shortness of breath (SOB) for the past two days. She reported the SOB began suddenly, was constant, and was exacerbated by movement and supine positioning. At previous baseline, she was fully functional and independent. She complained of recent weight gain, constipation, dry skin, and lower extremity swelling, but denied subjective fevers, cough, chest pain, and palpitations. Upon admission, she was in respiratory distress requiring oxygen supplementation via nasal cannula. Physical exam revealed reduced breath sounds and dullness to percussion at the lung bases and 2+ pitting edema in the lower extremities. She was afebrile with no leukocytosis. CXR reported moderate bilateral pleural effusions, with CTA confirmation ruling out PE. BNP, liver function tests, urine studies, albumin, and autoimmune workup was negative.The echocardiogram indicated normal right and left heart function and an elevated pulmonary artery systolic pressure of 57 mmHg. Thyroid function tests reported normal T4 level, mild low T3, and elevated TSH. Intravenous furosemide was initiated with rapid response and improvement. Attempted thoracentesis was unsuccessful in obtaining pleural fluid for analysis. Levothyroxine was initiated, and after two days of treatment, the patient demonstrated significant improvement in SOB, with an SpO2 99% on room air and resolution of edema. Follow-up CXR and CT revealed diminished pleural effusions and the patient was discharged without the need for oxygen supplementation. However, the patient returned to the hospital with the same complaint of SOB with bilateral pleural effusion three weeks after the first admission. On this admission, she underwent prompt thoracentesis, and 750 cc of yellow fluid was collected and submitted for fluid analysis. Fluid results were consistent with transudative pleural fluid and lymphocyte-predominant cells. These results and recurrent presentation, despite treatment of hypothyroidism, suggest that there may be an underlying etiology that still needs to be identified and treated.
Conclusion:
Subclinical hypothyroidism should be considered as a potential cause of bilateral pleural effusions when other potential causes have been ruled out, such as heart failure, liver and kidney dysfunction, and nephrotic syndrome. When this diagnosis is confirmed, treatment with levothyroxine and antidiuretics is recommended. However, this case demonstrates that early diagnostic closure can result in readmission for the same initial complaint of SOB from pleural effusion reaccumulation. Therefore, it’s crucial to maintain a broad differential diagnosis when investigating the underlying etiologies of persistent or worsening clinical complaints.
Academic/Professional Position
Medical Student
Academic/Professional Position (Other)
MS4
Recommended Citation
Chapman, Molly; Soto Abarca, Andrea; Ngo, Duc Khiem; and Ramos, Carlos T., "New Onset Bilateral Pleural Effusion: An Uncommon Presentation of Subclinical Hypothyroidism or a Premature Closure Diagnosis Error?" (2024). Research Symposium. 31.
https://scholarworks.utrgv.edu/somrs/2023/posters/31
Included in
New Onset Bilateral Pleural Effusion: An Uncommon Presentation of Subclinical Hypothyroidism or a Premature Closure Diagnosis Error?
Background: Subclinical hypothyroidism is biochemically defined with normal serum-free T4 in the presence of an elevated serum TSH. Common symptoms of an underactive thyroid can include fatigue, weakness, cold intolerance, weight gain despite poor appetite, hair loss, constipation, and depression. Pleural effusions have also been recognized as a clinical sequelae in the literature, where up to 25% of patients can develop a pleural fluid collection in the setting of hypothyroidism. Although not well understood, a mechanism includes an increased capillary permeability that leads to the retention of fluid in pleural cavities and other tissues.
Case presenting: A 66-year-old woman with PMH of hypertension and Type 2 DM presented to the hospital complaining of acute progressive shortness of breath (SOB) for the past two days. She reported the SOB began suddenly, was constant, and was exacerbated by movement and supine positioning. At previous baseline, she was fully functional and independent. She complained of recent weight gain, constipation, dry skin, and lower extremity swelling, but denied subjective fevers, cough, chest pain, and palpitations. Upon admission, she was in respiratory distress requiring oxygen supplementation via nasal cannula. Physical exam revealed reduced breath sounds and dullness to percussion at the lung bases and 2+ pitting edema in the lower extremities. She was afebrile with no leukocytosis. CXR reported moderate bilateral pleural effusions, with CTA confirmation ruling out PE. BNP, liver function tests, urine studies, albumin, and autoimmune workup was negative.The echocardiogram indicated normal right and left heart function and an elevated pulmonary artery systolic pressure of 57 mmHg. Thyroid function tests reported normal T4 level, mild low T3, and elevated TSH. Intravenous furosemide was initiated with rapid response and improvement. Attempted thoracentesis was unsuccessful in obtaining pleural fluid for analysis. Levothyroxine was initiated, and after two days of treatment, the patient demonstrated significant improvement in SOB, with an SpO2 99% on room air and resolution of edema. Follow-up CXR and CT revealed diminished pleural effusions and the patient was discharged without the need for oxygen supplementation. However, the patient returned to the hospital with the same complaint of SOB with bilateral pleural effusion three weeks after the first admission. On this admission, she underwent prompt thoracentesis, and 750 cc of yellow fluid was collected and submitted for fluid analysis. Fluid results were consistent with transudative pleural fluid and lymphocyte-predominant cells. These results and recurrent presentation, despite treatment of hypothyroidism, suggest that there may be an underlying etiology that still needs to be identified and treated.
Conclusion:
Subclinical hypothyroidism should be considered as a potential cause of bilateral pleural effusions when other potential causes have been ruled out, such as heart failure, liver and kidney dysfunction, and nephrotic syndrome. When this diagnosis is confirmed, treatment with levothyroxine and antidiuretics is recommended. However, this case demonstrates that early diagnostic closure can result in readmission for the same initial complaint of SOB from pleural effusion reaccumulation. Therefore, it’s crucial to maintain a broad differential diagnosis when investigating the underlying etiologies of persistent or worsening clinical complaints.