Case Presentation: A 70-year-old man with no significant history presented with lower back pain for 1 month. The pain, specifically involving the bilateral lower back which radiated down the buttocks, was sharp, intermittent, and 10/10 in severity. His pain started gradually but progressively worsened, limiting the patient’s ability to ambulate. The patient reported constipation for 4 days and urinary urgency, but he denied any trauma, fevers, chills, urinary or bowel incontinence, saddle anesthesia, weakness, numbness, or tingling. The patient denied any history of smoking or alcohol use. Initial evaluation was remarkable for an ESR of 46 (nl 0-22 mm/hr). A lumbar spine X-ray revealed chronic left L2 and L3 transverse processes fractures and a chronic appearing loss of L2 vertebral height. As the patient was thought to have musculoskeletal strain, the patient was conservatively treated with 2 doses of naproxen 500 mg PO, muscle relaxants, and a lidocaine patch and was referred for physical therapy. However given his pain remained uncontrolled for over 24 hours, an MRI of the lumbar spine was performed revealing an acute L2 vertebral body fracture with spinal cord compression. He was started on Dexamethasone (16 mg PO daily) and scheduled for surgical decompression. On hospital day 6 and day 4 of Dexamethasone, the patient developed malaise and vague epigastric/ right shoulder pain. Vital signs, physical exam, and KUB were normal. CT of the abdomen showed a large volume of extravasated contrast and free air within the lesser sac consistent with gastric perforation. He underwent emergent laparotomy but ultimately died 3 days later from multi-organ failure due to complications of the gastric perforation.
Discussion: This is an unfortunate case of gastric perforation induced by iatrogenic factors (i.e. minimal NSAID use followed by short term, high dose steroids) in a non-ICU patient without prior risk factors. Studies have shown that concomitant use of systemic steroids with specifically high doses of NSAIDs is associated with a 12-fold increased risk of upper gastrointestinal complications such as gastric perforation. Historically steroids frequently have been prescribed in association with acid suppressive therapy (AST), however there is no evidence suggesting benefits of concomitant use if no other risk factors exist. The American Society of Health-System Pharmacist (ASHP) guidelines even advise against stress ulcer prophylaxis in non-ICU hospitalized patients as well as ICU patients taking high dose steroids (>10 mg of Dexamethasone) without other risk factors. Based on current ASHP guidelines, our case did not meet criteria for stress ulcer prophylaxis as even though the patient was on high dose steroids, he had received only minimal NSAID treatment. Yet one can soundly speculate that AST as GI prophylaxis could have provided life saving benefit in this patient.
Conclusions: The above case highlights a patient who expired from a gastric perforation while on high dose steroids, yet only minimal NSAIDs. The combination of high dose steroids and high dose NSAIDS is well known to require acid suppressive therapy (AST) in order to provide gastrointestinal prophylaxis. Clinicians should thus be advised to consider short-term AST in patients on high dose steroids and minimal NSAID use as well.