Perioperative adrenal insufficiency presenting as refractory hypotension: A CARE-compliant article.
Adrenal insufficiency (AI) is a rare but potentially life-threatening cause of perioperative hemodynamic instability characterized by an inadequate cortisol response to physiological stress.
We report a case of a 77-year-old woman undergoing oblique lumbar interbody fusion who developed profound intraoperative hypotension refractory to fluid resuscitation and multiple vasopressors. Notably, she had a history of corticosteroid therapy for rheumatoid arthritis that had been discontinued nearly 3 decades earlier. She also exhibited extreme skin fragility.
AI was clinically suspected based on persistent vasopressor-resistant hypotension, a remote history of corticosteroid therapy, and extreme skin fragility.
Suspecting AI, intravenous hydrocortisone was administered postoperatively, resulting in rapid hemodynamic stabilization and subsequent weaning of vasopressors.
Pre- and postoperative biochemical testing was inconclusive for definitive AI. However, the clinical presentation and dramatic response to steroid administration strongly suggested surgical stress-related AI. The patient was discharged without any complications.
This case underscores the importance of maintaining a high index of suspicion for AI in patients with unexplained, vasopressor-resistant hypotension, even those with a remote history of corticosteroid use, as timely empirical treatment can be life-saving.
We report a case of a 77-year-old woman undergoing oblique lumbar interbody fusion who developed profound intraoperative hypotension refractory to fluid resuscitation and multiple vasopressors. Notably, she had a history of corticosteroid therapy for rheumatoid arthritis that had been discontinued nearly 3 decades earlier. She also exhibited extreme skin fragility.
AI was clinically suspected based on persistent vasopressor-resistant hypotension, a remote history of corticosteroid therapy, and extreme skin fragility.
Suspecting AI, intravenous hydrocortisone was administered postoperatively, resulting in rapid hemodynamic stabilization and subsequent weaning of vasopressors.
Pre- and postoperative biochemical testing was inconclusive for definitive AI. However, the clinical presentation and dramatic response to steroid administration strongly suggested surgical stress-related AI. The patient was discharged without any complications.
This case underscores the importance of maintaining a high index of suspicion for AI in patients with unexplained, vasopressor-resistant hypotension, even those with a remote history of corticosteroid use, as timely empirical treatment can be life-saving.