Abstract Introduction Corticosteroids are potent anti-inflammatory and immunosuppressive agents frequently used in short courses for various conditions. However, prolonged or inappropriate use can lead to severe complications, including immunosuppression, metabolic derangements, and delayed diagnosis of underlying disease. Cauda equina syndrome (CES) is a neurosurgical emergency that can be masked by corticosteroid therapy, while chronic use also predisposes to opportunistic infections such as Pneumocystis jirovecii pneumonia (PJP). We present a case of corticosteroid-induced hyperosmolar hyperglycemic state (HHS), PJP, and CES, illustrating systemic consequences of unsupervised steroid use. Case Description A 67-year-old male with COPD, cervical myelopathy, and hypertension presented with polyuria, polydipsia, and dyspnea. Laboratory studies revealed glucose 899 mg/dL, consistent with HHS. He was admitted to the ICU for insulin therapy and fluid resuscitation. On review, the patient reported self-administering 40mg of prednisone daily for two months after receiving over 1,000 tablets of 5mg prednisone over eight months. After stabilization, chest imaging revealed a cavitary lesion in the right upper lobe. Bronchoalveolar lavage grew Pseudomonas aeruginosa and Pneumocystis jirovecii. He was treated with cefepime and trimethoprim-sulfamethoxazole, and his steroids were gradually tapered. Following taper initiation, he developed new lower extremity weakness and bilateral groin pain. MRI revealed severe multilevel degenerative changes with cervical cord compression and findings consistent with CES. The patient underwent C4-T1 decompression and T12-L2 laminectomy. Postoperatively, he developed a wound infection requiring surgical revision and prolonged antibiotics before transfer to a tertiary center for further care. Discussion This case highlights the extensive and multifaceted complications of chronic corticosteroid use. Glucocorticoids induce hyperglycemia through increased gluconeogenesis, insulin resistance, and impaired glucose uptake, precipitating HHS even in non-diabetic individuals. Immunosuppression from long-term therapy predisposes patients to opportunistic infections such as PJP, while the anti-inflammatory effects may mask symptoms of neurologic emergencies like CES, delaying diagnosis and intervention. Additionally, impaired fibroblast function and angiogenesis contribute to delayed wound healing and postoperative infection. Conclusion Chronic corticosteroid use can precipitate life-threatening endocrine, infectious, and neurologic complications. Clinicians must exercise vigilance in prescribing and monitoring steroid therapy, ensure appropriate tapering and refill control, and provide patient education regarding risks of unsupervised use. This case underscores the need for a multidisciplinary approach to prevent and manage the systemic sequelae of corticosteroid overuse. This abstract is funded by: None
Grondel et al. (Fri,) studied this question.