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ODP472 Creation of the Anaplastic Care Team (ACT) protocol: Establishing a Benchmark for Timely Access to Care for Anaplastic Thyroid Cancer Patients
INTRODUCTION: Novel Coronavirus 19 (COVID19) has been shown to involve multiple organs. Its reported effects on the endocrine system have been via subacute thyroiditis, functional hypopituitarism, and triggering type 1 diabetes with ketosis. We describe a case of COVID19 infection presenting as adre...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9627505/ http://dx.doi.org/10.1210/jendso/bvac150.152 |
Sumario: | INTRODUCTION: Novel Coronavirus 19 (COVID19) has been shown to involve multiple organs. Its reported effects on the endocrine system have been via subacute thyroiditis, functional hypopituitarism, and triggering type 1 diabetes with ketosis. We describe a case of COVID19 infection presenting as adrenal insufficiency. CASE: A 35-year-old female with a history of developmental delay, anxiety, and hypothyroidism presented to the emergency department (ED) from her group home with complaints of abdominal pain and 2-3 episodes of nausea and vomiting per day for one week. She denied any changes in bowel habits, chest pain, shortness of breath. On physical examination, there was mild diffuse abdominal tenderness without any skin hyperpigmentation. In the ED, her vitals showed blood pressure 99/56, heart rate 94, respiratory rate 23, saturating at 100% on room air. Laboratory tests were remarkable for hyponatremia (sodium 123), hypokalemia (potassium 1.9), hypochloremia (chloride 88), hypophosphatemia (phosphorus 2), metabolic acidosis with bicarbonate of 14. Her COVID19 test was positive. She was admitted to the intensive care unit as her blood pressure continued to drop to as low as 76/37. Potassium, phosphorus was replaced, and normal saline infusion was started at 75ml/hr with minimal improvement in blood pressure to 94/53 and sodium to 126 in 24 hours. Urine electrolytes showed sodium <15, making SIADH less likely. On day 3, we suspected adrenal insufficiency due to persistent hypotension. Results showed am cortisol of 1 and ACTH of 10. ACTH stimulation test was unable to be done. She was started on hydrocortisone which improved her blood pressure as well as electrolytes. CT abdomen showed no adrenal abnormality. She was able to be tapered off the steroids in 2 weeks. CONCLUSION: COVID19 associated hypocortisolism presents both as primary and transient secondary adrenal insufficiency (via suppression of the hypothalamic-pituitary-adrenal axis, like in our case). Similar reversible hypocortisolism post-SARS infection was observed in 24 of 61 patients (39.3%) during the 2005 outbreak. Autopsy studies on patients with COVID19 showed adrenal necroptosis of the adrenal cortex. Although critical illness-related cortical insufficiency is not a new concept, the cortisol levels in COVID19 critically ill patients have been shown to be lower than non-COVID19 critically ill patients. Prompt addition of stress dose steroids can be lifesaving in critically ill COVID patients, especially when associated with resistant hypotension. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m. |
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