Abstract / Summary
Abstract Purpose Bilateral lower extremity edema is a common clinical symptom, often caused by cardiac, hepatic, renal, or venous disorders. However, the etiology of some refractory cases remains occult, and in such instances, lumbar spinal stenosis—a spinal etiology—is easily overlooked. Prolonged lower extremity edema secondary to lumbar spinal stenosis has rarely been reported in the literature, and the underlying pathophysiological mechanisms remain elusive.This case presents a unique instance where severe L4/5 lumbar spinal stenosis manifested solely as a five-year history of refractory bilateral calf edema, occurring in the complete absence of low back pain, sciatica, or neurogenic claudication. Notably, the edema resolved rapidly and completely following unilateral biportal endoscopic (UBE) decompression, providing direct in vivo evidence that stenosis-related edema is reversible after neural decompression. By documenting this rare presentation and its dramatic treatment response, this report aims to (1) raise awareness of a treatable spinal etiology in cryptogenic bilateral edema, (2) advocate for lumbar MRI as a screening modality, even in patients lacking overt spinal symptoms, and (3) provide mechanistic insights regarding epidural venous plexus compression and neurogenic inflammation, thereby expanding the etiological spectrum of lower extremity edema. Case Presentation A 76-year-old female presented with a five-year history of persistent symmetrical pitting edema of both calves, in the absence of low back pain, radicular pain, or motor deficits. Routine medical workup was unremarkable, with cardiac, hepatic, renal, and vascular etiologies excluded. Multiple therapeutic trials involving volume depletion strategies and diuretics proved ineffective. Subsequently, lumbar MRI and CT demonstrated severe lumbar spinal stenosis at the L4/L5 level. Results Following L4/5 unilateral biportal endoscopic (UBE) decompressive surgery (partial laminectomy with ligamentum flavum resection and central/lateral recess decompression under general anesthesia),bilateral calf edema markedly subsided on the first postoperative day and completely resolved by postoperative day 9.A repeat lower extremity ultrasound showed resolution of subcutaneous soft tissue edema in both calves.At the 4-week follow-up,no recurrence of lower extremity edema was observed. Conclusion This case illustrates that lumbar spinal stenosis represents a rare but reversible cause of refractory lower extremity edema. Proposed mechanisms may involve impaired venous return due to compression of the epidural venous plexus and potentially neurogenic inflammation. Lumbar MRI should be considered a screening tool for unexplained, refractory lower extremity edema. The UBE technique, as a minimally invasive and precise decompression approach, provides an effective treatment option for such patients and broadens the clinical understanding of the etiological spectrum of lower extremity edema.