Case reports in critical care · 2017
Acute-Onset Panhypopituitarism Nearly Missed by Initial Cosyntropin Testing.
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Blum Claudine A, Schneeberger Daniel, Lang Matthias, Rakic Janko, Michot Marc Philippe, Müller Beat
Аннотация
INTRODUCTION: Diagnosis of adrenal crisis and panhypopituitarism in patients with septic shock is difficult but crucial for outcome.
CASE: A 66-year-old woman with metastasized breast cancer presented to the ED with respiratory insufficiency and septic shock after a 2-day history of the flu. After transfer to the ICU, corticosteroids were started in addition to antibiotics, as the patient was vasopressor-nonresponsive. Diabetes insipidus was diagnosed due to polyuria and treated with 4 mg desmopressin. Thereafter, norepinephrine could be tapered rapidly. On day 2, basal cortisol was 136 nmol/L with an increase to 579 nmol/L in low-dose cosyntropin testing. Polyuria had not developed again. Therefore, corticosteroids were stopped. On day 3, the patient developed again nausea, vomiting, and polyuria. Adrenal crisis and diabetes insipidus were postulated. Corticosteroids and desmopressin were restarted. Further testing confirmed panhypopituitarism. MRI showed a new sellar metastasis. After 2 weeks, stimulated cortisol in cosyntropin testing reached only 219 nmol/l, confirming adrenal insufficiency.
DISCUSSION: The time course showed that the adrenal glands took 2 weeks to atrophy after loss of pituitary ACTH secretion. Therefore, a misleading result of the cosyntropin test in the initial phase with low basal cortisol and allegedly normal response to exogenous ACTH may be seen. Cosyntropin testing in the critically ill should be interpreted with caution and in the corresponding clinical setting.
CASE: A 66-year-old woman with metastasized breast cancer presented to the ED with respiratory insufficiency and septic shock after a 2-day history of the flu. After transfer to the ICU, corticosteroids were started in addition to antibiotics, as the patient was vasopressor-nonresponsive. Diabetes insipidus was diagnosed due to polyuria and treated with 4 mg desmopressin. Thereafter, norepinephrine could be tapered rapidly. On day 2, basal cortisol was 136 nmol/L with an increase to 579 nmol/L in low-dose cosyntropin testing. Polyuria had not developed again. Therefore, corticosteroids were stopped. On day 3, the patient developed again nausea, vomiting, and polyuria. Adrenal crisis and diabetes insipidus were postulated. Corticosteroids and desmopressin were restarted. Further testing confirmed panhypopituitarism. MRI showed a new sellar metastasis. After 2 weeks, stimulated cortisol in cosyntropin testing reached only 219 nmol/l, confirming adrenal insufficiency.
DISCUSSION: The time course showed that the adrenal glands took 2 weeks to atrophy after loss of pituitary ACTH secretion. Therefore, a misleading result of the cosyntropin test in the initial phase with low basal cortisol and allegedly normal response to exogenous ACTH may be seen. Cosyntropin testing in the critically ill should be interpreted with caution and in the corresponding clinical setting.